Annex XV dossier PROPOSAL FOR IDENTIFICATION OF A ... - ECHA

ANNEX XV – IDENTIFICATION OF SVHC 

Annex XV dossier 

PROPOSAL FOR IDENTIFICATION OF A SUBSTANCE AS A 

CMR CAT 1 OR 2, PBT, vPvB OR A SUBSTANCE OF AN 

EQUIVALENT LEVEL OF CONCERN 

Substance Name: Sodium chromate 

EC Number: 231-889-5 

CAS Number: 7775-11-3 

• It is proposed to identify the substance as a carcinogenic, mutagenic and toxic for reproduction 

substance according to Article 57 (a), (b) and (c). 

Submitted by: France 

Version: February 2010


CONTENTS 

CONTENTS .................................................................................................................................................................1 

TABLES .......................................................................................................................................................................3 

PART I: JUSTIFICATION...........................................................................................................................................5 

1 Identity of the substance and physical and chemical properties .....................................................................7 

1.1 Name and other identifiers of the substance........................................................................................7 

1.2 Composition of the substance..............................................................................................................8 

1.3 Physico-chemical properties................................................................................................................8 

2 Manufacture and uses .....................................................................................................................................9 

3 Classification and labelling.............................................................................................................................9 

4 Environmental fate properties.........................................................................................................................11 

5 Human health hazard assessment ...................................................................................................................11 

6 Human health hazard assessment of physico-chemical properties .................................................................12 

7 Environmental hazard assessment ..................................................................................................................12 

8 PBT, VPVB AND equivalent level of concern assessment............................................................................12 

PART II: INFORMATION ON USE, EXPOSURE, ALTERNATIVES AND RISKS ...............................................13 

1 Information on manufacture and uses.............................................................................................................14 

2 Information on exposure.................................................................................................................................15 

2.1 Exposure of workers............................................................................................................................15 

2.1.1 Global overview of workers exposure to chromium (VI) compounds in Europe..................15 

2.1.2 Workers exposure to sodium chromate specifically in Europe .............................................19 

2.2 Exposure of the general population via consumer products ................................................................19 

2.2.1 Dyestuffs ...............................................................................................................................19 

2.2.2 Leather goods ........................................................................................................................20 

2.3 Exposure of the general population via the environment ....................................................................20 

2.3.1 Exposure via drinking water..................................................................................................20 

2.3.2 Exposure via food..................................................................................................................20 

2.3.3 Exposure via ambient air.......................................................................................................20 

2.3.4 Exposure via the environment (water, sediment, soil and food chain)..................................21 

3 Information on alternatives.............................................................................................................................22 

4 Risk-related information.................................................................................................................................22 

OTHER INFORMATION ............................................................................................................................................23 

REFERENCES .............................................................................................................................................................24 

ANNEXES....................................................................................................................................................................26 

1 Annex I: Human health hazard assessment ....................................................................................................27 

1.1 Toxicokinetics (absorption, metabolism, distribution and elimination) ..............................................27 

1.2 Acute toxicity ......................................................................................................................................28 

1.3 Irritation...............................................................................................................................................28 

1


1.4 Corrosivity...........................................................................................................................................28 

1.5 Sensitisation ........................................................................................................................................29 

1.6 Repeated dose toxicity.........................................................................................................................29 

1.7 Mutagenicity........................................................................................................................................29 

1.7.1 In vitro data ...........................................................................................................................29 

1.7.2 In vivo data............................................................................................................................30 

1.7.3 Human data ...........................................................................................................................30 

1.7.4 Summary and discussion of mutagenicity.............................................................................30 

1.8 Carcinogenicity ...................................................................................................................................31 

1.8.1 Carcinogenicity: oral .............................................................................................................31 

1.8.2 Carcinogenicity: inhalation ...................................................................................................31 

1.8.3 Carcinogenicity: dermal ........................................................................................................31 

1.8.4 Carcinogenicity: human data.................................................................................................31 

1.8.5 Summary and discussion of carcinogenicity .........................................................................31 

1.9 Toxicity for reproduction ....................................................................................................................32 

1.9.1 Effects on fertility..................................................................................................................32 

1.9.2 Developmental toxicity .........................................................................................................33 

1.9.3 Human data ...........................................................................................................................36 

1.9.4 Summary and discussion of reproductive toxicity.................................................................36 

1.10 Other effects ........................................................................................................................................37 

1.11 Derivation of DNEL(s) or other quantitative or qualitative measure for dose response .....................37 

2 Annex II : Overall description of chromium manufacturing and chromium uses...........................................38 

2.1 Manufacture ........................................................................................................................................38 

2.2 Main applications and uses of chromium and chromium compounds referenced in literature............38 

2.2.1 Alloy and chromium metal production..................................................................................38 

2.2.2 Refractory applications..........................................................................................................38 

2.2.3 Chromium chemicals manufacturing and related uses ..........................................................39 

3 Annex III: Treatment and coating of metals, metal finishing processes using chromium (VI) compounds...42 

3.1 Formulation of metal treatment products ............................................................................................42 

3.2 Conversion coating (usually called chromate conversion coating – CCC) or chromating ..................42 

3.3 Sealing after anodising ........................................................................................................................43 

3.4 Chrome (electro)plating or chrome dipping or chroming...................................................................44 

3.4.1 Chrome plating methods .......................................................................................................44 

3.4.2 Chrome plating processes......................................................................................................45 

3.4.3 Brightening............................................................................................................................46 

4 Annex IV: Uses of chromium (VI) salts in the textile sector (process) ..........................................................47 

4.1 Dyeing of protein fibres ......................................................................................................................47 

4.2 Chemical reaction with fibre and dyestuff ..........................................................................................48 

4.3 Subsequent processes ..........................................................................................................................48 

2


TABLES 

Table 1: Summary of physico-chemical properties ......................................................................................................8 

Table 2: Risk Assessment for Lung Cancer..................................................................................................................16 

Table 3: Occupational Exposure Limits .......................................................................................................................17 

Table 4: Summary of occupational inhalation exposure data from the Risk Assessment Report.................................18 

Table 5: Summary of occupational dermal exposure data from the Risk Assessment Report......................................19 

3


PROPOSAL FOR IDENTIFICATION OF A SUBSTANCE AS A 

CMR CAT 1 OR 2, PBT, VPVB OR A SUBSTANCE OF AN 

EQUIVALENT LEVEL OF CONCERN 

Substance Name: Sodium chromate 

EC Number: 231-889-5 

CAS number: 7775-11-3 

• It is proposed to identify the substance as a carcinogenic, mutagenic and toxic for reproduction 

substance according to Article 57 (a), (b) and (c). 

Summary of how the substance meets the CMR (Cat 1 or 2), PBT or vPvB criteria, or is 

considered to be a substance of an equivalent level of concern 

According to Article 57 of Regulation 1907/2006 (the REACH Regulation), substances meeting the 

criteria for classification as carcinogenic (category 1 or 2), as mutagenic (category 1 or 2) or as 

toxic for reproduction (category 1 or 2) in accordance with Council Directive 67/548/EEC may be 

included in Annex XIV. 

Sodium chromate has been classified as a carcinogenic (Carc. Cat. 2), as a mutagenic (Muta. Cat. 2) 

and as a reprotoxic (Repr. Cat. 2) according to Commission Directive 2004/73/EC of 29 April 2004 

adapting to technical progress for the twenty-ninth time Council Directive 67/548/EEC on the 

approximation of the laws, regulations and administrative provisions relating to the classification, 

packaging and labelling of dangerous substances. The corresponding classification in Annex VI of 

Regulation (EC) No 1272/2008 adopted on 10 August 2009 is Carc. 1B, Muta. 1B and Repr. 1B. 

Consequently, sodium chromate has to be considered as a substance meeting the criteria of Article 

57 (a), of Article 57 (b) and of Article 57 (c) of the REACH Regulation. 

Registration number(s) of the substance or of substances containing the substance: not 

available 

4


PART I: JUSTIFICATION 

5


This report covers only sodium chromate. The risk related to chromium (VI) compounds has 

already been assessed in the Risk Assessment Report (RAR) published in 2005 (E.C., 2005) and 

which focused on chromium trioxide, sodium chromate, sodium dichromate, potassium dichromate 

and ammonium dichromate. Sodium dichromate is already included in the candidate list. 

Three other Annex XV reports are submitted jointly and concern potassium dichromate, potassium 

chromate and ammonium dichromate. Part I of each report is similar (except for potassium 

chromate which is not classified as toxic for reproduction) since information comes from the Risk 

Assessment Report. 

Common background description of chromium, chromate and dichromate compounds 

Chromium is a member of the transition metals, in group 6. Chromium(0) is the metallic form 

(metallic chromium Cr) and is essentially inert. Chromium exhibits a wide range of possible 

oxidation states. The most common oxidation states of chromium are (+2), (+3), and (+6). 

Chromium (II) is the divalent form (oxidation state (+2)): such chromous compounds include 

chromous chloride (CrCl2) and chromous sulfate (CrSO4). 

Chromium (III) is the trivalent form (oxidation state (+3)) which is the most stable. Chromium (VI) 

is the hexavalent form which refers to chemical compounds that contain the element chromium in 

the (+6) oxidation state. 

Chromium (VI) (or Cr (VI)) is most commonly encountered as oxospecies in the (mono)chromate 

(CrO4 2− ) and dichromate (Cr2O7 2− ) anions which are strong oxidising agents at low pH. Their 

oxidative property is widely used in organic chemistry. Chromates and dichromates are salts of 

chromic acid and dichromic acid, respectively. Chromic acid, which is an oxacid has the 

hypothetical structure H2CrO4. By loosing two protons (H + ), chromic acid and dichromic acid form 

chromate ion and dichromate ion respectively. Neither chromic nor dichromic acid can be isolated, 

but their anions are found in a variety of compounds: the chromates and dichromates. The dark red 

chromium (VI) oxide CrO3 (chromium trioxide) is the acid anhydride of chromic acid and it is sold 

industrially as “chromic acid”. 

Chromate salts contain the chromate anion CrO4 2− , and usually have an intense yellow color. 

Dichromate salts contain the dichromate anion Cr2O7 2− , and usually have an intense orange color. 

By comparison, the chromates and dichromates of heavy metals (such as silver and lead) often have 

a red color. 

In aqueous solution, hexavalent chromium exists as hydrochromate HCrO4 − , chromate CrO4 2− , and 

dichromate Cr2O7 2− ionic species. Chromate anion tends to dimerize in dichromate. The proportion 

of each ion in solution is pH dependent. In basic and neutral pH, the chromate form predominates. 

As the pH is lowered (6.0 to 6.2), the hydrochromate concentration increases. At very low pH, the 

dichromate species predominate (US-EPA, 1998). Under particular conditions, a polymerisation can 

occur leading to the production of polychromates with the following formula CrnO3n+1 2- . 

Main chromium forms are the following according to their oxidation state: 

Chromium metals and alloys (Cr (0)): 

Chromium metal 

Stainless steel 

Other chromium containing alloys 

Divalent (Cr (2+)): 

6


Chromous chloride CrCl2 

Chromous sulfate CrSO4 

Trivalent (Cr (3+)): 

Chromic oxide Cr2O3 

Chromic chloride CrCl3 

Chromic sulfate Cr2(SO4) 3 

Chromic potassium sulphate KCr(SO4) 2 

Chromite ore FeO.Cr2O3 

Hexavalent (Cr (6+)) chromate : 

Chromium trioxide CrO3 

Chromic acid H2CrO4 

Sodium chromate Na2CrO4 

Potassium chromate K2CrO4 

Zinc chromate ZnCrO4 

Strontium chromate SrCrO4 

Hexavalent (Cr (6+)) dichromate : 

Sodium dichromate Na2Cr2O7 

Potassium dichromate K2Cr2O7 

Ammonium dichromate (NH4)2Cr2O7 

Zinc dichromate ZnCr2O7 

1 IDENTITY OF THE SUBSTANCE AND PHYSICAL AND CHEMICAL 

PROPERTIES 

1.1 Name and other identifiers of the substance 

Chemical Name: Sodium chromate 

EC Number: 231-889-5 


IUPAC Name: Disodium chromate 

Synonyms: Sodium monochromate, Disodium chromium tetraoxide 

7


1.2 Composition of the substance 

Chemical Name: Sodium chromate 

EC Number: 231-889-5 


IUPAC Name: Disodium chromate 

Molecular Formula (Hill) Na2CrO4 

Molecular Formula (CAS): CrH2O4.2Na 

Structural Formula: 

Molecular Weight: 161.99 g/mol 

Typical concentration (% w/w): 99 % (typical impurities: none stated) 

Impurities are not known. 

1.3 Physico-chemical properties 

The following information on physico-chemical properties was taken from the Risk Assessment 

Report on chromium compounds, published by the ECB in 2005 (E.C., 2005). 

Physico-chemical parameters such as boiling point, octanol-water partition coefficient and vapour 

pressure have little meaning for solid ionic inorganic compounds. 

Table 1: Summary of physico-chemical properties 

REACH ref 

Annex, § 

Property Value 

VII, 7.1 Physical state at 20°C and 

101.3 kPa 

Slightly deliquescent yellow crystals in 

hydrated form (usually tetra or deca hydrated) 

VII, 7.2 Melting/freezing point (°C) Decahydrate loses H2O and melts at ~20°C; 

anhydrous salt melts at ~762°C 

VII, 7.3 Boiling point n/a: inorganic ionic compound 

VII, 7.4 Relative density ~2.4 - 2.7 

VII, 7.5 Vapour pressure n/a: inorganic ionic compound 

VII, 7.7 Water solubility at 20°C (g/L) ~530 (the aqueous solution is alkaline (pH 9)) 

VII, 7.8 Partition coefficient noctanol/water 

(log value) 

n/a: inorganic ionic compound 

8


2 MANUFACTURE AND USES 

Information on manufacture and uses may be useful for prioritisation of substances for inclusion in 

Annex XIV but this should be summarised under section 1 of the second part of this report. 

3 CLASSIFICATION AND LABELLING 

According to Article 57 of Regulation 1907/2006 (the REACH Regulation), substances meeting the 

criteria for classification as carcinogenic (category 1 or 2), as mutagenic (category 1 or 2) or as 

toxic for reproduction (category 1 or 2) in accordance with Council Directive 67/548/EEC may be 

included in Annex XIV. 

Sodium chromate has index number 024-018-00-3 in Annex VI, part 3, Tables 3.1 and 3.2 of 

Regulation (EC) No 1272/2008. 

Sodium chromate is classified in Annex VI (part 3, Tables 3.1 and 3.2) of Regulation (EC) No 

1272/2008 on classification, labelling and packaging of substances and mixtures, amending and 

repealing Directives 67/548/EEC and 1999/45/EC, and amending Regulation (EC) No 1907/2006. 

Its classification according to part 3 of Annex VI, Table 3.2 (the list of harmonised classification 

and labelling of hazardous substances from Annex I to Council Directive 67/548/EEC) of 

Regulation (EC) No 1272/2008 is: 

9


Classification Labelling Concentration 

Limits 

Carc. Cat. 2; 

T+; N 

R42/43: C ≥ 0.2 % E 

R45 

Muta. Cat. 2; 

R: 45-46-60-61-21-25-26-34-42/43- 

48/23-50/53 

3 

R46 

Repr. Cat. 2; 

R60-61 

T+; R26 

T; R25-48/23 

Xn; R21 

C; R34 

R42/43 

N; R50-53 

S: 53-45-60-61 

Key: 

Carc.: Carcinogenic; Muta: Mutagenic; Repr.: Toxic for reproduction 

R21: Harmful in contact with skin 

R25: Toxic if swallowed 

R26: Very toxic by inhalation 

R34: Causes burns 

R42/43: May cause sensitization by inhalation and skin contact 

R45: May cause cancer 

R46: May cause heritable genetic damage 

R48/23: Toxic: danger of serious damage to health by prolonged exposure through inhalation 

R50-53: Very toxic to aquatic organisms, may cause long-term adverse effects in the aquatic environment 

R60: May impair fertility 

R61: May cause harm to the unborn child 

T+: Very toxic 

T: Toxic 

Xn: Harmful 

C: Corrosive 

N: Dangerous for the environment 

S53: Avoid exposure - obtain special instructions before use 

S45: In case of accident or if you feel unwell, seek medical advice immediately (show the label where possible) 

S60: This material and its container must be disposed of as hazardous waste 

S61: Avoid release to the environment. Refer to special instructions/Safety data sheets 

Note E : Substances with specific effects on human health that are classified as carcinogenic, mutagenic and/or toxic for 

reproduction in categories 1 or 2 are ascribed Note E if they are also classified as very toxic (T+), toxic (T) or harmful 

(Xn). For these substances, the risk phrases R20, R21, R22, R23, R24, R25, R26, R27, R28, R39, R68 (harmful), R48 

and R65 and all combinations of these risk phrases shall be preceded by the word ‘Also’. 

Note 3 : The concentration stated is the percentage by weight of chromate ions dissolved in water calculated with 

reference to the total weight of the mixture 

Notes 

10


Its harmonised classification according to part 3 of Annex VI, Table 3.1 of Regulation (EC) No 

1272/2008 is: 

Hazard Class and 

Category Code(s) 

Carc. 1B 

Muta. 1B 

Repr. 1B 

Acute Tox. 2 * 


STOT RE 1 


Skin Corr. 1B 

Resp. Sens. 1 

Skin Sens. 1 

Aquatic Acute 1 

Aquatic Chronic 1 

Classification Labelling 

Hazard 

statement 

Code(s) 

H350 

H340 

H360-FD 

H330 

H301 

H372** 

H312 

H314 

H334 

H317 

H400 

H410 

Pictogram, 

Signal 

Word Code(s) 

GHS06 

GHS08 

GHS05 

GHS09 

Dgr 

Hazard 

statement 

Code(s) 

H350 

H340 

H360FD 

H330 

H301 

H372 ** 

H312 

H314 

H334 

H317 

H410 

Specific Conc. 

Limits, 

M-factors 

Resp. Sens.; 

H334: C ≥ 0.2 % 

Skin Sens.; H317: 

C ≥ 0.2 % 

Key: 

Carc. 1 B: Carcinogenicity; Muta. 1B: Germ cell mutagenicity; Repr. 1B: Reproductive toxicity; Acute Tox. 2, Tox. 3, 

Tox. 4: Acute toxicity ; STOT RE 1 : Specific target organ toxicity — repeated exposure; Skin Corr. 1B: Skin 

corrosion/irritation; Resp. Sens. 1 : Respiratory/skin sensitization ; Skin Sens. 1: Respiratory/skin sensitization 

Aquatic Acute 1, Aquatic Chronic 1: Hazardous to the aquatic environment 

H301: Toxic if swallowed 

H312: Harmful in contact with skin 

H314: Causes severe skin burns and eye damage 

H317: May cause an allergic skin reaction 

H330: Fatal if inhaled 

H334: May cause allergy or asthma symptoms or breathing difficulties if inhaled 

H350: May cause cancer 

H340: May cause genetic defects 

H360-FD: May damage fertility. May damage the unborn child 

H372**: Causes damage to organs through prolonged or repeated exposure 

H400: Very toxic to aquatic life 

H410: Very toxic to aquatic life with long lasting effects 

GHS05: Corrosion 

GHS06: skull and crossbones 

GHS08: Health hazard 

GHS09: Environment 

Dgr: Danger 

Note 3: The concentration stated is the percentage by weight of chromate ions dissolved in water calculated with 

reference to the total weight of the mixture 

An asterisk (*) indicates: Minimum classification for a category 

Asterisks (**) indicate: Route of exposure cannot be excluded 

4 ENVIRONMENTAL FATE PROPERTIES 

Not relevant for this dossier. 

5 HUMAN HEALTH HAZARD ASSESSMENT 

Please refer to Annex I to get an informal overview of the human health hazard assessment on 

chromium compounds (chromium trioxide, sodium dichromate, sodium chromate, ammonium 

3 

Notes 

11


dichromate and potassium dichromate) from the Risk Assessment Report (E.C., 2005) and from 

other sources regarding the irritation, corrosion and sensitisation effects. 

6 HUMAN HEALTH HAZARD ASSESSMENT OF PHYSICO-CHEMICAL 

PROPERTIES 


7 ENVIRONMENTAL HAZARD ASSESSMENT 


8 PBT, VPVB AND EQUIVALENT LEVEL OF CONCERN ASSESSMENT 


12


PART II: INFORMATION ON USE, EXPOSURE, ALTERNATIVES 

AND RISKS 

13


1 INFORMATION ON MANUFACTURE AND USES 

A global overview of chromium and chromium compounds manufacturing and uses is given in 

Annex II. 

Following information concerns specifically sodium chromate (or other chromates when data on 

sodium chromate are not available). 

Sodium chromate is the first chemical produced from chromite ore in the manufacture of chromate 

chemicals. The ore, containing approximately 30% chromium, is first dried, crushed and ground in 

ball mills. Sodium chromate is made by alkaline (sodium carbonate) oxidation in kilns at 

temperatures in the range of 1,000-1,200°C. After about 4 hours the reacted material leaving the 

kilns is either crushed and cooled before extraction of the water soluble components or quenched 

directly to form slurry containing sodium chromate, aluminate and vanadate in the aqueous phase. 

The slurry is conditioned to precipitate soluble alumina before separating the unreacted mineral 

residue, some of which is recycled to the kiln process after drying to aid extraction efficiency. The 

chromate solution is passed through other conditioning stages to remove soluble impurities. For 

example, sodium hydroxide and calcium hydroxide are used to precipitate soluble vanadium 

impurities as calcium vanadate. The latter is removed by pressure filtration and excess calcium is 

precipitated as the carbonate by treatment with sodium carbonate. At this stage, the partially 

purified solution contains around 35% sodium chromate (E.C., 2005). 

According to the Risk Assessment Report (E.C., 2005), global world production capacities for 

sodium chromate have been estimated by the industry at 910 kT/year. 

EU production (without import) of sodium chromate was estimated in 1997 around 103,000 tons 

per year (E.C., 2005). No more detailed and aggregated information on volumes imported and used 

in Europe is available. 

The annual importation of chromate, dichromate and peroxochromate (excluded: zinc or lead 

chromate and sodium dichromate) in France was estimated at 1286 tons and the annual exportation 

was estimated at 7 tons in 2005 (INRS, 2005). According to INRS, sodium chromate is no more 

used in France. 

In the Risk Assessment Report it is mentioned that sodium chromate is mainly used in manufacture 

of other chromium compounds (E.C., 2005) (see Figure A1 in Annex II). According to the Industry 

(French consultation, 2010), sodium chromate is used as an analytical reagent in laboratories; 

however, this use is limited. 

The US Department of Defense (ASETSDefense, 2010) mentioned that sodium chromate is used in 

conversion coatings and as a corrosion inhibitor in cooling systems. These uses have not been 

checked currently at the European level. For more information on treatment and coating of metals, 

metal finishing processes using chromium (VI) compounds, please refer to Annex III. 

Other potential uses referenced in literature (HSDB, 2005) are the following: 

- chemical intermediate for pigments and catalysts, 

- corrosion inhibitor (sealed water in cooling systems, oil-well drilling muds, protection of 

iron), 

- mordant for dyes, dying paint pigment (in manufacture of pigments/inks), 

14


- drilling mud additive, 

- component of cells for chlorate manufacture, 

- leather tanning, 

- by making use of Cr-51 isotope, sterile sodium chromate (VI) solution is used in 

pharmaceuticals for the determination of circulatory red cell volume, cell survival time and 

evaluation of blood lose. 

- aluminium etchant ingredient. 

All these referenced uses have not been checked currently at the European level. 

According to Industry, sodium chromate was removed from paint stripper and cutting fluid in the 

aeronautic sector (French consultation, 2010). 

This Annex XV report focused on the potential use of sodium chromate as an analytical reagent in 

laboratories and as an intermediate in manufacture of other chromium compounds as it has not been 

possible to check the other uses at the European level. 

2 INFORMATION ON EXPOSURE 

From 2007, coatings containing hexavalent chromium will no longer be permitted under the End of 

Life Vehicles Directive (Directive 2000/53/EC of the European Parliament and of the Council of 18 

September 2000 on end-of life vehicles) and the Waste Electrical and Electronic Equipment 

Directive (Directive 2002/96/EC of the European Parliament and of the Council of 27 January 2003 

on waste electrical and electronic equipment). This will impact on some of the passivation 

applications where Cr (VI) is present in the finished articles and substitution will become a 

necessity. 

In addition, Migration limits have been established within Council Directive 2009/48/EC, for the 

presence of chromium (VI) in children’s toys. 

Considering that chromium compounds are no more manufactured in Europe (cf. section 2.1 in 

Annex II), workers exposure related to the manufacturing of chromium (VI) compounds is not 

expected. 

2.1 Exposure of workers 

2.1.1 Global overview of workers exposure to chromium (VI) compounds in Europe 

Several million workers worldwide are exposed to airborne fumes, mists and dust containing 

chromium or its compounds. Of the occupational situations in which exposure to chromium occurs, 

highest exposures to chromium (VI) may occur during chromate production, welding, chrome 

pigment manufacture, chrome plating and spray painting. Highest exposures to other forms of 

chromium occur during mining, ferrochromium and steel production, welding and cutting and 

grinding of chromium alloys (IARC, 1997). 

Data on exposure levels are available for several specific industries and job categories covering 

several decades. In the past, exposures to chromium (VI) in excess of 1 mg/m 3 were found 

repeatedly in some processes, including chromium plating, chromate production and certain 

welding operations; exposures to total chromium have been even higher. Modern control 

technologies have markedly reduced exposures in some processes, such as electroplating, in recent 

years (IARC, 1997). 

15


In epidemiological studies on cancer in humans, clearly and consistently elevated lung cancer risks 

have been observed in chromate production (exposure mainly to trivalent and water-soluble 

hexavalent chromium compounds), in chromate pigment production (exposure mainly to watersoluble 

and water-insoluble chromates) and also in chromium plating using chromic acid (ICDA, 

2001). 

A recent recommendation from the Scientific Committee on Occupational Exposure Limits 

(SCOEL) concluded that lung cancer was the critical effect of concern for occupational exposure, 

such that controls aimed at reducing lung cancer should also reduce the risk of other effects 

(SCOEL, 2004). In view of the genotoxicity of Cr (VI) compounds, it is not possible to identify a 

clear threshold below which there would be no increased risk of lung cancer. Consequently, no 

conclusions were reached concerning the magnitude of the cancer risk in workers. However, the 

recommendation from SCOEL has been published containing quantitative risk estimates for lung 

cancer. Table 2 shows the quantitative risk estimates for lung cancer as presented in the 

SCOEL/SUM/86 final document (SCOEL, 2004). 

Table 2: Risk Assessment for Lung Cancer 

Excess lung cancer cases per 1000 

male workers 

Exposure (Working Lifetime 

to a range of Cr (VI) compounds) 

5-28 0.05 mg/m 3 

2-14 0.025 mg/m 3 

1-6 0.01 mg/m 3 

0.5-3 0.005 mg/m 3 

0.1-0.6 0.001 mg/m 3 

The values in the Table 2 are based on an analysis of 10 epidemiological studies and were derived 

using a linear no-threshold model. SCOEL agreed that such a linear extrapolation approach was 

appropriate given that the Cr (VI) compounds are comprehensively genotoxic. It is important to 

note that the SCOEL report draws attention to areas of uncertainty associated with these risk 

estimates. For example, SCOEL felt that the irritant and inflammatory properties of the Cr (VI) 

compounds might contribute to the carcinogenic process. Such effects are likely to have dose 

thresholds, and hence the modelled risk values may be over-estimated at low exposures. In addition, 

SCOEL noted that at low exposures to Cr (VI) compounds, there are physiological defence 

mechanisms in the lungs that can convert Cr (VI) to the less harmful trivalent forms of chromium. 

This again suggests that a linear model may overestimate risks at low exposures. In essence, the 

SCOEL report presents risk estimates derived using a linear no-threshold model, but on the other 

hand, also includes toxicological reasons why the model could lead to an overestimation of lung 

cancer risk at low levels of exposure. Therefore, although the risk estimates are presented here for 

information, the uncertainties surrounding them must not be overlooked. 

Overall, the SCOEL SUM recommends that for the soluble chromates (VI), consideration could be 

given to setting an occupational exposure limit at either 0.01 mg/m 3 or 0.025 mg/m 3 (8-hour TWA). 

There are a number of countries with exposure limits for chromates and these have been tabulated 

below (E.C., 2005). These limits are provided for information and not as an indication of the level 

of control of exposure achieved in practice in workplaces in these countries. 

16


Table 3: Occupational Exposure Limits 

Country Compound 

Limit 

(mg/m 3 as Cr) 

Type of Limit 

UK Cr (VI) compounds 0.05 8-hour TWA (MEL) 

Germany 

USA ACGIH 

Production of soluble Cr (VI) 

compounds 

Other Cr (VI) compounds 

Water soluble Cr (VI) 

compounds 

0.1 

0.05 

USA OSHA Cr (VI) compounds 0.1 (as CrO3) 

USA NIOSH Cr (VI) compounds 0.001 

Netherlands Soluble Cr (VI) compounds 

Sweden Chromates and chromic acid 

8-hour TWA (TRK) 

0.05 8-hour TWA (TLV) 

0.025 

0.05 

0.02 

0.06 

STEL/ceiling 

(PEL) 

TWA (REL) 

10-hour workday 

40-hour workweek 

8-hour TWA 

STEL 

8-hour TWA 

STEL 

Finland Cr (VI) compounds 0.05 TWA 

Japan 

Cr (VI) compounds – 

carcinogenic 

forms 

Cr (VI) compounds 

France Cr (VI) compounds 

Key: 

MEL: Maximum exposure limit 

NIOSH: National Institute for Occupational Safety and Health 

PEL: Permissible exposure limit 

OSHA: Occupational Safety and Health Administration 

REL: Recommended exposure limit 

STEL: Short term exposure limit 

TLV: Threshold limit value 

TRK : Technical exposure limit 

TWA: Time weighted average 

0.01 

0.05 

0.05 

0.1 

8-hour TWA 

8-hour TWA 

8-hour TWA 

STEL 

For information, the Occupational Safety and Health Administration (OSHA) proposed to tighten 

the standard for hexavalent chromium occupational exposure with a permissible exposure limit 

(PEL) value for chromium (VI) of 0.005 mg/m 3 (calculated as an 8-hour time-weighted average 

(TWA)) (OSHA, 2008). 

Values of Occupational exposure limits (OELs) are broadly similar across the EU. However there 

may be differences across Member States in relation to the legal or advisory framework associated 

with OELs affecting the way OELs are interpreted and complied with. These proposed occupational 

exposure limits only relate to inhalation exposure. Occupational exposure limits are not usually set 

for dermal exposure. 

17


As the bronchial tree is the primary target organ for carcinogenic effects of Cr (VI), inhalation of 

chromium-containing aerosols is therefore a major concern with respect to exposure to chromium 

compounds. The Risk Assessment Report on chromium compounds provides inhalation exposure 

data for Cr (VI) compounds for different industry sector (E.C., 2005). These data are summarised in 

the Table 4. Reasonable worst-case (RWC) inhalation exposures are based on the 90 th percentile of 

available measured data with professional judgment used where limited data were available. 

Table 4: Summary of occupational inhalation exposure data from the Risk Assessment Report 

Industry 

Number of 

samples 

Range of 

exposures 

(mg/m 3 ) 

Geometric 

mean 

(mg/m 3 ) 

Reasonable 

worst case (RWC) 

(mg/m 3 ) 

Source 

Manufacture of the five chromates 1,889 nd-0.78 0.004 0.02 measured data 

Manufacture of other Cr 

containing chemicals 

- dyestuffs 39 nd-1.4 0.02 

- chrome tan 

115 0.00001 - 

0.025 

0.5 (8 hours) 

1.5 (short term) 

measured data 

judgement 

0.002 0.007 measured data 

Inhalation exposure data on manufacturing process are given only for information as chromium 

compounds are no more manufactured in Europe (see Annex II). 

The manufacturing process for the five chromates is largely enclosed with breaching for bagging of 

product and some maintenance activities. The measured exposure data indicate that inhalation 

exposures for operators are usually very low, with those for maintenance staff and packers slightly 

higher. Exposures during the manufacture of the five chromates range from none detected to 0.78 

mg/m 3 . A reasonable worst-case exposure is 0.02 mg/m 3 , based on the 90 th percentile of the 

industry data for 1994-1997 for Company 1 (see the Risk Assessment Report for more information). 

There are two types of chromium pigments: those that remain as chromium (VI) and those which 

are reduced to chromium (III). For both types, exposures usually occur during weighing and mixing 

of ingredients. Once they have been mixed and reacted then there is no further exposure. The range 

of exposures is quite large, from none detected to 1.4 mg/m 3 . It seems likely that the high exposures 

were obtained when local exhaust ventilation (LEV) was not in use. A reasonable worst-case 

exposure of 0.5 mg/m 3 was agreed. For short term exposures a RWC is 1.5 mg/m 3 (E.C., 2005). In 

manufacture of pigments and dyes, although there are a number of companies in the EU, the exact 

number of workers involved is unknown. 

For few plants which continue to use Cr (VI) compounds for tanning use, chrome salts are made 

either by reacting sodium dichromate with sulphur gas in an enclosed process or by reacting sodium 

dichromate and sodium chromate with a reducing sugar. In both cases liquid chromates are used and 

exposures will be low as there is little potential for exposure except when liquid chromate is 

discharged from a road tanker into a storage vessel. The production process itself takes place in an 

enclosed system. The range of exposures is 0.00001 - 0.025 mg/m 3 . A reasonable worst-case 

exposure is 0.007 mg/m 3 , based on the 90 th percentile of the available data (E.C., 2005). The exact 

numbers of workers involved in the manufacture of chromium (VI) tanning agents is unknown but 

expected to be low since chromium (III) sulphate is now commonly used for this purpose. 

18


The Risk Assessment Report on chromium compounds also provides dermal exposure data for Cr 

(VI) compounds for different industry sector (E.C., 2005). These data are summarised in the Table 

5. The EASE (Estimation and Assessment of Substance Exposure) model was used to predict 

dermal exposures during the manufacture of chromates. 

Table 5: Summary of occupational dermal exposure data from the Risk Assessment Report 

Industry 

Range of exposures 

(mg/cm 2 /day) 

Source 

Manufacture of the 5 chromates 0 - 0.1 EASE 

Manufacture of other Cr containing 

chemicals 

- dyestuffs 0.1 - 1 EASE 

- chrome tan 0 - 0.1 EASE 

Dermal exposure data on manufacturing process are given only for information as chromium 

compounds are no more manufactured in Europe (see Annex II). 

In the manufacture of the five chromate compounds dermal exposures were predicted to be 0 to 0.1 

mg/cm 2 /day during packing operations. It was not possible to predict dermal exposures during 

maintenance operations because of lack of information. Personal Protective Equipment (PPE) is 

worn during all manufacturing stages. PPE, properly selected and worn will significantly reduce 

exposure. 

In the manufacture of other chromium-containing chemicals dermal exposures most often occur 

during weighing and charging of reactants to vessels. In the manufacture of dyestuffs dermal 

exposure is predicted to be 0.1-1 mg/cm 2 /day. In chrome tan manufacture dermal exposures are 

predicted to be 0-0.1 mg/cm 2 /day (E.C., 2005). 

2.1.2 Workers exposure to sodium chromate specifically in Europe 

No information available. 

2.2 Exposure of the general population via consumer products 

Chromium (VI) compounds are not known to be present in greater than residual concentrations in 

products available directly to the consumer (E.C., 2005). 

2.2.1 Dyestuffs 

According to the Italian Textile and Health Association (Associazione Tessile e Salute, 2009) 

hexavalent chromium can be present in textiles which are dyed with post-chromating dyes when 

chromating conditions are not properly checked. Today, it is object of investigation in textiles, but 

the overall analyses made showed that it has been detected in very rare cases. Moreover, the Italian 

production, through the addition of a reduction after dyeing, ensures the absence of Cr (VI) in the 

textile product (see Annex IV for more information on the textile dyeing process using chromates). 

19


2.2.2 Leather goods 

Concerning leather goods, most of the tanning within the EU is carried out using basic trivalent 

chromium (III) sulphate. Basic trivalent chromium sulphate manufactured within the EU contains 

no measurable Cr (VI) (Cross H.J. et al., 1997). Consequently, consumer exposure to Cr (VI) from 

leather goods based on leather tanned within the EU is expected to be insignificant. 

A French study (Martinetti R., 1994) has demonstrated that under specific conditions of humidity, 

ultraviolet-C light and pH, there is a possibility of transforming chromium (III) compounds into 

chromium (VI) compounds which could migrate from the leather. However research is still needed 

to better understand the transformation mechanism of chromium (III) to chromium (VI) in finished 

leather as well as the potential toxic effects to man at this very low range of values. 

Considering that health problems with chromium are mostly related to leather products (chromium 

is also found in textile products like dyed wool and silk), the German enforcement authorities 

strongly advise all those marketing leather products in Germany to ensure that the Cr (VI) content 

of the leather does not exceed 3 ppm which is the detection limit (CBI, 2008). 

2.3 Exposure of the general population via the environment 

Nonoccupational sources of exposure to chromium include food, air and water, but the levels are 

usually several orders of magnitude lower than those typically encountered in occupational 

situations (IARC, 1997). 

Releases of chromium (VI) from any sources are expected to be reduced to chromium (III) in most 

situations in the environment. The impact of chromium (VI) as such is therefore likely to be limited 

to the area around the source (E.C., 2005). 

2.3.1 Exposure via drinking water 

The concentration of chromium in water varies according to the type of the surrounding industrial 

sources and the nature of the underlying soils (WHO, 2000). For example, in the Netherlands, the 

chromium concentration of 76% of the supplies was below 1 µg/L and of 98% below 2 µg/L 

(WHO, 2003). As far as drinking water quality and consumer protection is concerned WHO and the 

European Union (under the Council Directive 98/83/EC of 3 November 1998 on the quality of 

water intended for human consumption) have established a guideline value of 50 µg/L for total 

chromium in drinking water (WHO, 2003). 

2.3.2 Exposure via food 

Food contains chromium at concentrations ranging from


Ranges of chromium levels in Member States of the European Union were given as follows: remote 

areas: 0-3 ng/m 3 , urban areas: 4-70 ng/m 3 and industrial areas: 5-200 ng/m 3 , e.g. the mean 

concentration of total chromium in air in the Netherlands varied from 2 to 5 ng/m 3 (WHO, 2003). 

Mass median diameters of chromium-containing particulates in ambient air have been reported to 

be in the range 1.5–1.9 µm (WHO, 2000). According to the EPA (US-EPA, 1998), chromium 

particles of small aerodynamic diameter (< 10 µm) will remain airborne for a long period. 

Consequently, population may be exposed to chromium through inhalation of ambient air. 

The retention of chromium compounds from inhalation, based on a 24-hour respiratory volume of 

20 m 3 in urban areas with an average chromium concentration of 50 ng/m 3 , is about 3–400 ng. 

Individual uptake may vary depending on concomitant exposure to other relevant factors, e.g. 

tobacco smoking, and on the distribution of the particle sizes in the inhaled aerosol (WHO, 2000). 

Mean chromium intakes (estimated total exposure) from food and water range from 52 to 943 

µg/day (WHO, 2003). The estimated total intake of chromium from air, water, and food by the 

general population in the United Kingdom is in the range 78–106 µg/day. Food contributed 93–98% 

of the total intake and water 1.9–7%. The contribution from air was negligible. In the Netherlands, 

the estimated mean daily chromium intake is 100 µg, with a range of 50–200 µg. In general, food 

appears to be the major source of intake. Drinking-water intake can, however, contribute 

substantially when total chromium levels are above 25 µg/L. 

2.3.4 Exposure via the environment (water, sediment, soil and food chain) 

The following information on exposure via the environment was taken from the Risk Assessment 

Report on chromium compounds, published by the ECB in 2005 (E.C., 2005). 

They are potential releases to water as some of the processes take place in water. Then released, the 

behaviour of chromium species in the environment can be influenced by environmental factors, 

such as pH and water hardness. 

In the Risk Assessment Report on chromium compounds, it was assumed that for acidic (or neutral, 

where high concentrations of reductants for chromium (VI) exist) soils, sediments and waters, 

chromium (VI) will be rapidly reduced to chromium (III) and that 3% of the chromium (III) formed 

will be oxidised back to chromium (VI). The net result of this is that of the estimated chromium 

(VI) release to the environment, 3% will remain as chromium (VI) and 97% will be converted to 

chromium (III). Consequently, exposure to chromium (VI) in the environment is expected to be 

reduced by the formation of chromium (III). 

Under less favourable conditions, e.g. alkaline conditions (~pH>8) and/or neutral conditions, where 

low concentrations of reductants for chromium (VI) exist, it will be assumed that the rate of 

reduction of chromium (VI) to chromium (III) is slow, with a long half-life of around 1 year. Such 

conditions are found in seawater, where a pH of around 8 is typical. 

In addition, chromium (VI) exists mainly as highly soluble oxoanions in the environment and is 

expected to be mobile in soils and sediments although its adsorption is pH dependent. As a 

consequence, exposures through soils and sediments are not likely to be significant. 

Moreover, there are no direct emissions to land, although the particulate emissions to air are likely 

to be deposited to land. Sludge application is another potential route to land; however, from 

comments from producers and users it is more usual for solid waste and sludges to be disposed of to 

landfill. 

21


Chromium (VI) has been shown to be taken up by a wide range of organisms from water, sediment 

and soil. For fish, although uptake does occur, the bioconcentration factors for chromium (VI) are 

usually very low (~1 L/kg). However, the uptake of chromium by other organisms appears to be 

higher than seen for fish, although few of the experiments distinguish between chromium (VI) and 

chromium (III) concentrations in the organisms. Similar to the situation for fish, it is possible that 

once taken up by the organism, chromium (VI) is reduced to chromium (III) in the tissues, resulting 

in a build up of chromium (III) and hence an overestimate for the true bioconcentration factor for 

chromium (VI). BCFs of up to around 9,100 L/kg (on a mussel dry weight basis) for chromium (VI) 

and 2,800 L/kg (on a mussel dry weight basis) for chromium (III) have been determined in mussels, 

and BCFs of around 500 L/kg (on a cell dry weight basis) for chromium (VI) and 12,000-130,000 

L/kg (on a cell dry weight basis) for chromium (III) have been determined in algae. Transfer of 

chromium via the alga to bivalve, and sediment to bivalve food chains appears to be relatively low. 

However, in the Risk Assessment Report on chromium compounds, it was concluded that further 

work could be done to test whether the mussel-based food chain is of concern. 

3 INFORMATION ON ALTERNATIVES 

No data available 

4 RISK-RELATED INFORMATION 

In relation to human health related with chromium (VI) compounds, the Risk Assessment Report 

conducted in 2005 (E.C., 2005) concluded that further measures were needed to limit the risks for 

workers, consumers and humans via the environment, and that risk reduction measures which are 

already being applied shall be taken into account. 

In view of the genotoxic and carcinogenic properties of chromium (VI) the report concludes that 

there are concerns for all exposure scenarios. In addition, there are concerns for acute toxicity as a 

result of short-term peak exposures, for skin and eye irritation, respiratory tract sensory irritation, 

skin sensitisation, occupational asthma and reproductive toxicity (fertility and developmental 

toxicity). Therefore, these concerns are relevant for all chromates as well. 

Applying the existing workplace health and safety legislation can lead to adequate control of the 

inhalation risks of exposure to chromium (VI) compounds, assuming that the adequate control is 

defined as reducing the exposure to below 0.01 mg/m 3. . Even if it seems possible to reduce 

inhalation exposure below 0.01 mg/m 3 , this exposure average can however not be technically 

consistently maintained. Furthermore, some exposures (dermal route in particular) remain 

insufficiently monitored. At last, other concerns remain for health risks at this level of exposure. 

22


Consultation of the industry 

OTHER INFORMATION 

A closed consultation focused on sodium chromate has been conducted at both the French and the 

European levels from the 18 th December 2009 to the 15 th January 2010, which has completed a 

previous French consultation on all chromium (VI) compounds. 

Comments and technical contributions have been received from the following industrial sectors: 

- chemical companies federation (UIC), 

- reagents and chemicals manufacturing (Carlo Erba Reactifs, Daiichi-sankyo), 

- pharmaceutical industry (Valdepharm), 

- metal production (French ores, industrial minerals and non ferrous metals Federation; 

French steel Federation), 

- mechanical industry (Technical centre for mechanical industry), 

- civil and military aircraft manufacturing (French aerospace industries association, Airbus 

industry, Eurocopter-EADS), 

- metal finishing (French metal finishing trade union), 

- nuclear power industry, 

- wood production for construction (OBBIA, CEI-Bois), 

- building materials manufacturing (Delachaux), 

- textile manufacturing and finishing (Italian Textile and Health Association), 

- etc. 

Grouping approach of chromium (VI) compounds 

Regarding the potential inclusion of several chromium (VI) compounds in the Annex XIV of 

REACH (“authorization list”) and according ECHA’s approach on substances prioritisation 1 , a 

grouping approach seems justified in order to prevent simple replacement of a substance that will be 

subjected to authorisation by another form of the substance which will not. 

Indeed, some shared uses have been identified amongst chromium (VI) compounds (especially in 

the metal finishing sector) and it appears possible within the same process to easily replace one 

compound by another of the same family (sodium dichromate and potassium dichromate for 

instance). Moreover it appears possible to produce on-site a compound which may be subjected to 

authorisation from another one, by relevant chemical processes. 

1 General Approach for Prioritisation of Substances of Very High Concern (SVHCs) for Inclusion in the List of 

Substances Subject to Autorisation. Document developed in the context of ECHA’s first Recommendation for the 

inclusion of substances in Annex XIV - 1 June 2009. 

23


REFERENCES 

ASETSDefense. (2010). ASETSDefense (Advanced Surface Engineering Technologies for a 

Sustainable Defense) answer to AFSSET (French agency for environmental and occupational health 

safety) consultation on chromate compounds, 14 January 2010. 

Associazione Tessile e Salute. (2009). Associazione Tessile e Salute answer to AFSSET (French 

agency for environmental and occupational health safety) consultation on chromate compounds, 03 

December 2009. 

Bastarache E. (2010). Information taken from the Ceramicstoday website on January 2010 - link: 

http://www.ceramicstoday.com/articles/chrome_english.htm. 

CBI. (2008). Germany legislation: Chromium in leather and textile products (additional 

requirement). Information taken from the CBI Market Information Database available on this 

website: www.cbi.eu. 

Cross H.J., Faux S.P., Sadhra S. et al. (1997). Criteria Document for Hexavalent Chromium 

Commissioned by International Chromium Development Association (ICDA), Paris, France. 

E.C. (2005). European Union Risk Assessment Report - Chromium trioxide (CAS-No: 1333-82-0), 

sodium chromate (CAS-No:7775-11-3), sodium dichromate (CAS-No: 10588-01-9), ammonium 

dichromate (CAS-No: 7789-09-5) and potassium dichromate (CAS-No: 7778-50-9) Risk 

Assessment. 415 p. (EUR 21508 EN - Volume: 53). 

Elbetieha A., Al-Hamood M.H. (1997). Long-term exposure of male and female mice to trivalent 

and hexavalent chromium compounds: effect on fertility. Toxicology; 116(1-3):39-47. 

HSDB. Hazardous Substances Data Bank. (2005). http://toxnet.nlm.nih.gov/cgibin/sis/htmlgen?HSDB> 

IARC. (1997). International Agency for Research on Cancer (IARC) Monographs on the evaluation 

of carcinogenic risks to humans - Volume 49 - Chromium, Nickel and Welding - Summary of data 

reported and evaluation. 

ICDA. (1998). Chromium in Timber Preservation. The chromium file n°5. Website - link: 

http://www.icdachromium.com/pdf/publications/crfile5nov98.htm. 

ICDA. (2001). Health effects of occupational exposures in chrome plating. The chromium file n°7. 

Website - link: http://www.icdachromium.com/pdf/publications/crfile7dec01.htm. 

INRS. (2005). Inventaire 2005 des agents CMR - Fiche du chromate de sodium (CAS n°7775-11- 

3). Website - link: 

http://chat.inrs.fr/cmr/publigen_cmr_v2.nsf/FrontOffice?OpenFrameset&Start=D:CAS_7775-11-3. 

Junaid M., Murthy C.M., Saxena D.K. (1996a). Embryotoxicity of orally administered chromium in 

mice: Exposure during the period of organogenesis. Toxicology Letters; 84(3):143-148. 

24


Junaid M., Murthy R.C., Saxena D.K. (1996b). Embryo- and fetotoxicity of chromium in 

pregestationally exposed mice. Bull. Environ. Contam. Toxicol.; 57(3):327-334. 

Martinetti R. (1994). Thèse: Contribution à la labellisation "écoproduit" de cuirs tannés aux sels de 

Chrome : étude de la mobilité du Chrome, Lyon-France : CTC, 27 October 1994. 

OSHA. (2008). Information taken from the Occupational Safety and Health Administration website 

- link: http://www.osha.gov/. 

SCOEL. (2004). Recommendation from the Scientific Committee on Occupational Exposure 

Limits: Risk assessment for Hexavalent chromium. (SCOEL/SUM/86). 

Trivedi B., Saxena D.K., Murthy R.C. et al. (1989). Embryotoxicity and fetotoxicity of orally 

administered hexavalent chromium in mice. Reproductive Toxicology; 3(5):275-278. 

US-EPA. (1998). Toxicological review of hexavalent chromium (CAS No 18540-29-9) in support 

of summary information on the integrated risk information system (IRIS). 70 p. 

US-EPA. (2000). Hazard summary on Chromium compounds on the US-EPA website - link: 

http://www.epa.gov/ttn/atw/hlthef/chromium.html. 

WHO. (2000). World Health Organization (WHO) air quality guidelines for Europe - 2nd edition. 

WHO. (2003). Chromium in drinking-water - background document for development of World 

Health Organization (WHO) Guidelines for drinking-water quality. (WHO/SDE/WSH/03.04/04). 

25


ANNEXES 

26


1 Annex I: Human health hazard assessment 

This annex is given for information only. An Annex XV report on SVHC identification is indeed 

not the place to discuss the already agreed classification of sodium chromate. Its content is however 

a useful background in support to part II of this report. 

Most of the following information are taken from the Risk Assessment Report on chromium 

compounds (chromium trioxide, sodium dichromate, sodium chromate, ammonium dichromate and 

potassium dichromate), published by the ECB in 2005 (E.C., 2005). Please refer to the original 

document for more detailed information. It is likely that potassium chromate has not been 

prioritised for this risk assessment either because of a different hazard classification (considering 

that this substance is not classified reprotoxic contrary to the five other chromates) either because of 

less significant volumes and uses. 

However, considering that all chromate/dichromate ions produced from Cr (VI) compounds will 

behave similarly in biological tissues, other than the additional property of acidity and its potential 

influence on toxicity for chromium (VI) trioxide, it is assumed that all the Cr (VI) compounds can 

be treated as a common group. 

According to the hazard summary from the US EPA (US-EPA, 2000), the respiratory tract is the 

major target organ for chromium (VI) toxicity, for acute (short-term) and chronic (long-term) 

inhalation exposures. Shortness of breath, coughing, and wheezing were reported from a case of 

acute exposure to chromium (VI), while perforations and ulcerations of the septum, bronchitis, 

decreased pulmonary function, pneumonia, and other respiratory effects have been noted from 

chronic exposure. Epidemiological studies raise concerns for the carcinogenic potential of the Cr 

(VI) compounds. Animal studies have shown chromium (VI) to cause lung tumors via inhalation 

exposure. 

1.1 Toxicokinetics (absorption, metabolism, distribution and elimination) 

There is a reasonably good database available on the toxicokinetics of the Cr (VI) compounds under 

review, although there are relatively few human data. The available data indicate that generally Cr 

(VI) compounds are likely to behave in a similar manner in respect of toxicokinetics, and that the 

kinetic behaviour of these substances would be similar in those species studied, including humans. 

Following inhalation exposure, animal studies have shown that 20-30% of the administered Cr (VI) 

is absorbed via the respiratory tract. Highly water-soluble Cr (VI) is poorly absorbed via the 

gastrointestinal tract (only 2-9% of the dose was absorbed in human studies) due to reduction to the 

relatively poorly absorbed Cr (III). Only limited dermal absorption takes place through intact skin, 

with 1-4% Cr (VI) from an aqueous solution crossing the skin in guinea pig studies. 

According to results of animal testing, chromium species derived from these compounds can remain 

in the lungs for several weeks after inhalation exposure and also becomes bound to hemoglobin in 

erythrocytes for the lifespan of the cells. Part of Cr (VI) becomes reduced to Cr (III) after entering 

the body due to the influence of reducing agents, for example glutathione. Distribution is 

widespread even after a single dose and includes transfer of absorbed Cr (VI) across the placenta. 

Excretion occurs in urine and faeces. Repeated exposure leads to accumulation of chromium in 

several tissues, particularly the spleen because of uptake of senescent erythrocytes. 

27


1.2 Acute toxicity 

Highly water-soluble Cr (VI) compounds are very toxic by inhalation and toxic by ingestion. The 

respiratory tract and the kidney are damaged by these compounds following inhalation and oral 

exposure respectively. Although acutely harmful or toxic by the dermal route, more severe 

responses may be observed due to greater uptake via the skin if there is any prior or simultaneous 

damage to the skin. Depending upon the pH of the Cr (VI) solution, corrosive effects can occur on 

contact (see section 1.4 on corrosivity). 

1.3 Irritation 

Single application of a low concentration of highly water-soluble Cr (VI) in solution to undamaged 

human skin resulted in only a mild irritant response around the hair follicles. Animal data indicate 

that irritation occurs following single application to the skin for 4 hours. It is not possible to 

determine a clear concentration-response relationship for human skin irritation from the singleexposure 

animal or occupational data available. Repeated-exposure skin responses are considered 

under corrosivity (see section 1.4 on corrosivity). 

Significant damage to the eye can occur upon accidental exposure to highly water-soluble Cr (VI) 

compounds. Severe and persistent effects occur when there is contact with the low pH aqueous 

chromium (VI) trioxide or Cr (VI) solutions at high temperature. A number of case reports have 

detailed both inflammation of the cornea and conjunctivae and in more severe cases, corneal 

erosion and ulceration. The severity of response is increased by low pH or high temperature. 

Accidental eye contact with the corrosive aqueous chromium (VI) trioxide results in conjunctival 

congestion and necrosis and corneal oedema and opacity. It is not possible to determine a clear 

concentration-response relationship from the data available. 

In a very poorly-reported volunteer study, 10 subjects were apparently exposed to chromium (VI) 

trioxide at concentrations of 10-24 mg/m 3 (5-12 mg Cr (VI)/m 3 ) for “brief periods of time”. It was 

claimed that this exposure caused nasal irritation. According to the authors, exposure to lower but 

unspecified concentrations produced slight if any irritation of the upper respiratory tract. Given the 

poor reporting in this study the results cannot be considered to be reliable. 

Symptoms of sensory irritation of the respiratory tract are known to occur among chrome plating 

workers exposed to a mist of aqueous chromium (VI) trioxide. Since this is corrosive, such 

symptoms are to be expected. No quantitative data on such irritation are available from studies of 

workers. No studies reporting symptoms of sensory irritation are available for the other Cr (VI) 

compounds. Overall, it is not possible to determine a reliable concentration-response relationship 

for respiratory tract irritation using the available data. 

1.4 Corrosivity 

Highly water-soluble Cr (VI) compounds can cause very severe skin effects under certain 

conditions. In workers repeatedly exposed to highly water-soluble Cr (VI), where there is some 

slight initial damage to the skin, ulcers can develop which constitute a serious and persistent effect. 

Animal data are consistent with the observations made in humans. It is not possible to determine a 

clear concentration-response relationship for repeated-exposure human skin effects from the 

occupational data available and quantitative data could be misleading given the potential for severe 

effects resulting from repeated contamination of slightly damaged skin. Overall, highly watersoluble 

Cr (VI) compounds should be regarded as corrosive. 

28


1.5 Sensitisation 

Skin sensitisation resulting from contact with Cr (VI) is relatively common in humans working with 

the compounds. This has been demonstrated in patch testing of contact dermatitis patients and in 

investigations of various occupational groups. In addition, skin sensitisation potential has been 

clearly demonstrated in standard and modified guinea pig maximisation tests and in the mouse ear 

swelling test. 

Current understanding of the mechanism involved in the sensitisation indicates that Cr (III) is the 

ultimate hapten. Skin contact with Cr (VI) leads to penetration of Cr (VI) into the skin where it is 

reduced to Cr (III). There is some evidence for cross-reactivity between Cr (III) and Cr (VI); Cr 

(VI)-sensitised subjects may also react to Cr (III). Overall, it is not possible to reliably determine a 

threshold for either induction or challenge in an exposed population using the available data. 

According to Ceramicstoday (Bastarache E., 2010), hexavalent chromium can penetrate the skin 

where it is reduced to trivalent chromium which plays the role of an hapten; when fixed on a 

protein, it becomes a complete antigen. Chromate sensivity has proved fairly persistent once 

developed. Contact with textiles colored with chromate-based pigments can be sufficient to 

exacerbate the dermatitis. The wearing of leather shoes tanned with chromates can produce 

dermatitis of the feet if these are allowed to remain sweaty. In sensitized individuals, the absorption 

of chromium by pulmonary and/or oral way could cause an exzematous reaction. After cutaneous 

exposure to chromic acid, erosions of the skin may occur. These « chrome holes » initially appear 

as papular lesions, either singly or grouped, with central ulceration. 

The available case reports and evidence from well-conducted bronchial challenge tests, show that 

inhalation of Cr (VI) compounds can cause occupational asthma. As with skin, Cr (VI) - sensitised 

subjects may react to Cr (III). It is not possible to determine a no-effect level or exposure-response 

relationship for induction or elicitation of occupational asthma. 

1.6 Repeated dose toxicity 

Please refer to sections 1.4 and 1.5. 

1.7 Mutagenicity 

1.7.1 In vitro data 

There is a very large body of evidence indicating that the Cr (VI) ion in solution is directly 

mutagenic in in vitro systems. Extensive in vitro testing of highly water-soluble Cr (VI) compounds 

has produced positive results for point mutations and DNA damage in bacteria, point mutations, 

mitotic crossing-over, gene conversion, disomy and diploid in yeasts, and gene mutation, DNA 

damage, chromosome aberrations, sister chromatid exchanges and unscheduled DNA synthesis in 

mammalian cells. 

The in vitro genotoxicity of Cr (VI) was diminished considerably by the presence of reducing 

agents, in the form of tissue S9 or S12 fractions, gastric juice or reducing agents such as 

glutathione, ascorbate or sulphite. These all serve to reduce Cr (VI) to Cr (III) outside the cell 

therefore greatly reducing entry of chromium into the cell. 

29


1.7.2 In vivo data 

The genotoxicity of Cr (VI) compounds in vivo has been less extensively studied. Parenteral 

administration of sodium or potassium dichromate or potassium chromate to rats or mice resulted in 

significant increases in chromosome aberrations and micronucleated cells in the bone marrow and 

DNA single-strand breaks, interstrand cross-links and DNA-protein cross-links in the liver, kidneys 

and lung. A mouse spot test involving intraperitoneal injection of potassium chromate gave positive 

results. Oral studies have been negative but these employed lower dose levels and absorption is 

known to be poor by the oral route. Overall, water soluble Cr (VI) compounds are in vivo somatic 

cell mutagens in animal studies. 

A significant increase in post implantation deaths in a dominant lethal assay was reported in mice 

following intraperitoneal injection of potassium dichromate. Toxicokinetic data for water-soluble 

Cr (VI) compounds indicate that chromium will reach the germ cells following inhalation exposure 

(i.e. a relevant route of exposure for humans). Therefore taking these two observations together, it 

can be concluded that water-soluble Cr (VI) compounds have the potential to produce germ cell 

mutagenicity. 

1.7.3 Human data 

A few studies have been conducted in which circulating lymphocytes have been isolated from 

chromium-exposed workers and examined for chromosome aberrations, micronuclei, sister 

chromatid exchanges (SCE) and changes in chromosome numbers. In general, the results from 

better-conducted and reported studies including chromium plating workers in Japan and SS-MMA 

(manual metal arc on stainless steel) welders in Scandinavia have been negative. 

Evidence of genotoxicity has been reported in several other studies of chromate production workers 

in Eastern Europe and chromium plating workers in Italy. However the manner in which these were 

conducted and reported precludes full assessment of the significance of the findings. 

1.7.4 Summary and discussion of mutagenicity 

Few studies of genotoxic potential in humans are available. No evidence of genotoxic activity has 

been found in adequately-conducted studies in circulating lymphocytes from chromium exposed 

workers. In contrast, there is a vast array of genotoxicity data in vitro and less extensive testing in 

animals available. The evidence clearly indicates that highly water-soluble Cr (VI) compounds can 

produce significant mutagenic activity in vitro and in vivo. The Cr (VI) compound under 

consideration is therefore regarded as in vivo somatic cell mutagen. In addition, toxicokinetic and 

dominant lethal data suggest that water-soluble Cr (VI) has the potential to be an in vivo germ cell 

mutagen. For information and according to the American Conference of Governmental Industrial 

Hygienists (ACGIH) (Bastarache E., 2010), water-soluble hexavalent chromium compounds 

include: chromic acid, chromic acid anhydrides, monochromates and dichromates of sodium, of 

potassium, of ammonium, of lithium, of cesium, of rubidium. Water-insoluble hexavalent 

chromium compounds include: zinc chromate, calcium chromate, lead chromate, barium chromate, 

strontium chromate and sintered chromium trioxide. 

30


1.8 Carcinogenicity 

1.8.1 Carcinogenicity: oral 

No data available. 

1.8.2 Carcinogenicity: inhalation 

A few animal carcinogenicity studies were available. Results indicated that sodium dichromate was 

clearly carcinogenic, producing lung tumours when administered to rats by continuous inhalation of 

aqueous aerosol or long-term repeated intratracheal instillation in saline. Also, there was a single 

incidence of a squamous cell carcinoma of the pharynx after inhalation of sodium dichromate 

aerosol in rats. 

In rats and mice, inhalation studies using an aerosol or mist of chromium (VI) trioxide produced 1-2 

test group animals with lung tumours where such were mainly absent among corresponding 

controls. These studies suffered from some deficiencies in design such as small group size or 

inadequate dosing regimes. In two intrabronchial implantation studies in the rat, 1-2 animals with 

carcinomas of the respiratory tract were found in chromium (VI) trioxide-treated groups. No 

respiratory tract tumours were observed in controls in these studies. 

1.8.3 Carcinogenicity: dermal 

No data available. 

1.8.4 Carcinogenicity: human data 

A number of epidemiology studies investigated cancer risks among workers exposed to various 

forms of Cr (III) and Cr (VI). Unfortunately, detailed analysis of smoking habits is almost 

invariably absent. In chromate production, workers are exposed to Cr (III) during the production of 

Cr (VI) in water-soluble form e.g. sodium chromate. Although studies of chromate production have 

clearly established that there is an increase in lung cancer mortality, it is not clear precisely which 

Cr (VI) compound(s) produced the effect. An excess risk of lung cancer mortality has also been 

reported for workers in the chromate pigment production industry. However, this industry involves 

exposure to sparingly soluble or poorly soluble zinc or lead chromates as well as the sodium 

dichromate. 

Overall, it was concluded that chromium (VI) trioxide in solution is a human carcinogen but only 

limited information is available for the other Cr (VI) compounds. 

1.8.5 Summary and discussion of carcinogenicity 

Epidemiology data from chromate production, chromium pigment manufacture and other 

chromium-exposed groups showing clear increases in lung cancers cannot be specifically related to 

exposure to Cr (VI) compounds. However, it is highly probable that Cr (VI) ions in solution were 

the ultimate carcinogenic entity in these situations. Hence these epidemiological studies raise 

concerns for the carcinogenic potential of the Cr (VI) compounds. 

In animal carcinogenicity studies, sodium dichromate was carcinogenic in rats, causing lung tumour 

production, when given by repeated long term inhalation or intratracheal instillation. In rats and 

31


mice, inhalation or intrabronchial implantation studies using chromium (VI) trioxide produced 1-2 

test group animals with lung tumours where such were mainly absent among corresponding 

controls. Thus, in animal studies there is some evidence of respiratory tract carcinogenic activity for 

sodium dichromate and chromium (VI) trioxide. Similar studies in rats using other Cr (VI) 

compounds, able to produce Cr (VI) in solution, produced carcinogenicity in the lung. Hence there 

is good reason from animal studies to be concerned about the carcinogenic potential of the Cr (VI) 

compounds, in terms of the inhalation route and the respiratory tract as a site of action. Data for the 

oral and dermal routes and carcinogenicity studies on the Cr (VI) compounds are not available. 

Chromium (VI) compounds might be expected to have potential to cause cancer on repeated oral or 

dermal exposure. In the case of the oral route, any systemic carcinogenic potential could be limited 

by poor absorption of Cr (VI), and reduction to Cr (III) within the gastrointestinal tract although site 

of contact activity would remain an issue. Similar considerations apply to the skin. 

Overall, therefore, the Cr (VI) compounds are considered to have proven or suspect carcinogenic 

potential. From the available information, and taking into account the genotoxic potential of these 

substances, it is not possible to identify any dose-response relationship or thresholds for this effect. 

1.9 Toxicity for reproduction 

1.9.1 Effects on fertility 

The effects of potassium dichromate on male and female fertility were investigated in sexually 

mature (7 weeks old) Swiss mice administered this hexavalent chromium compound in drinking 

water (Elbetieha A. and Al-Hamood M.H., 1997). Groups of 9-20 males were administered 0, 

1,000, 2,000, 4,000 or 5,000 mg/L potassium dichromate equivalent to doses of approximately 0, 

166, 333, 666, 833 mg/kg/day (0, 60, 120, 235, 290 mg Cr (VI)/kg/day) for 12 weeks and then 

mated for ten days, 1 male to 2 untreated females. The exposed males were then removed and 1 

week later the females were terminated. Similarly, groups of 11-18 females were administered 0, 

2,000 or 5,000 mg/L potassium dichromate equivalent to doses of approximately 0, 400, 1,000 

mg/kg/day (0, 140, 350 mg Cr (VI)/kg/day) for 12 weeks and then mated for ten days, 3 females to 

1 untreated male. One week after the removal of the males, the females were terminated. Number of 

pregnant females, total implantations, viable fetuses and resorptions were recorded. In addition, 

satellite groups of 10-13 males and 8-10 females administered 0, 2,000 (males only) or 5,000 mg/L 

potassium dichromate for 12 weeks were sacrificed at the end of the treatment. Body and 

reproductive organ weights were recorded in these animals. No explanation is provided in the study 

report concerning the variability in group size. Also, it is unclear how dose levels were selected. 

At higher concentrations, the treated animals consumed less water per day compared to the control 

group (no more details provided). It is unclear whether or not the dose was adjusted for the reduced 

water consumption or if these animals received a lower dose. There were no deaths or clinical signs 

of toxicity in any group of male or female mice exposed. Compared to the control group, a 

statistically significant reduction in absolute body weight of 10% and 12% was seen in satellite 

group males at 2,000 and 5,000 mg/L (the only two dose levels at which body weight was 

recorded), respectively. Body weight of satellite group females administered 5,000 mg/L potassium 

dichromate (the only dose at which body weight was recorded) was unaffected. Relative testes 

weights were statistically significantly increased at 2,000 (by 17.5%) and 5,000 mg/L (by 21.5%). 

Relative seminal vesicles and preputial gland weights were statistically significantly reduced at 

5,000 mg/L only (by 27% and 34%, respectively). A statistically significant increase in relative 

ovarian weight (by 50%) was reported at 5,000 mg/L. It is noted that in the absence of information 

on the absolute organ weights, the increase seen in relative testis weight could be accounted for by 

32


the reduction in absolute body weight observed in males. It is also noted that, in the absence of 

histopathological examinations, it is difficult to interpret the toxicological significance of these 

organ weight changes. 

Compared to the control groups, the percentage of pregnant unexposed females mated with treated 

males and of pregnant exposed females mated with untreated males was unaffected by the 

treatment. The mean number of implantation sites was statistically significantly reduced in females 

impregnated by males treated with 2,000 (6.33 versus 8.18 in the control group) and 4,000 mg/L 

potassium dichromate (6.86 versus 8.18), but not with the highest dose (7.84 versus 8.18). Given 

the absence of a dose-response relationship, the toxicological significance of this finding is 

uncertain. However, it is possible that at higher concentrations, the actual doses the animals 

received were lower than the nominal doses, due to the reduced water consumption. There were no 

resorptions and dead fetuses in the control group and in the females impregnated by males treated 

with 2,000 or 4,000 mg/L potassium dichromate. However, 3 resorptions were noted in the females 

impregnated by males treated with the lowest dose (1,000 mg/L). Given the absence of a clear doseresponse 

relationship and that it is not clearly reported whether these findings occurred in one single 

litter or in different litters, the 3 resorptions seen at 1,000 mg/L are regarded as being incidental. A 

total number of 6 resorptions and of 6 dead fetuses was also observed in the females impregnated 

by males treated with the highest dose (5,000 mg/L). Although it is not reported whether these 

findings occurred in one single litter or in different litters, given the incidence, it is unlikely they 

occurred in one isolated litter. Hence, the fetolethality reported at this dose level (5,000 mg/L) is 

regarded as being treatment-related. The mean number of implantations and of viable fetuses was 

also statistically significantly reduced in females treated with 2,000 mg/L (7.35 versus 9.00 and 

6.55 versus 8.76, respectively) and 5,000 mg/L potassium dichromate (7.44 versus 9.00 and 5.88 

versus 8.76, respectively). There was also a statistically significant increase in the number of 

pregnant females with resorptions at 2,000 (53% versus 11%) and at 5,000 mg/L (63% versus 11%). 

Similarly, a total number of 37 and 14 resorptions (versus 4 in the control group) were observed at 

2,000 and 5,000 mg/L, respectively. 

Overall, the results of this study indicate that oral administration of potassium dichromate to mice 

for 12 weeks produced adverse effects on male and female fertility (reduced number of 

implantations) at 2,000 mg/L (333 mg/kg/day (120 mg Cr (VI)/kg/day) and 400 mg/kg/day (140 mg 

Cr (VI)/kg/day) in males and females, respectively) and above. These effects occurred, for the 

males, at dose levels at which a significant reduction in absolute body weight was noted. In the 

females, no effects on body weight were noted, but at the highest dose of 1,000 mg/kg/day (350 mg 

Cr (VI)/kg/day) there was a significant increase in relative ovarian weight. A NOAEL for these 

fertility effects of 1,000 mg/L (equivalent to 166 mg/kg/day potassium dichromate or 60 mg Cr 

(VI)/kg/day) was identified in males from this study. No NOAEL value was determined for the 

females as these fertility effects (reduced number of implantations) were reported even at the lowest 

dose tested of 2,000 mg/L (equivalent to 400 mg/kg/day potassium dichromate or 140 mg Cr 

(VI)/kg/day). A reduced number of viable fetuses and an increased number of resorptions were 

observed in females treated with 2,000 and 5,000 mg/L (400 and 1,000 mg/kg/day (140 and 350 mg 

Cr (VI)/kg/day)). In addition, an increased number of resorptions and dead fetuses were seen in 

untreated females impregnated by males given the highest dose of 5,000 mg/L (833 mg/kg/day (290 

mg Cr (VI)/kg/day). 

1.9.2 Developmental toxicity 

In a developmental toxicity study (Trivedi B. et al., 1989), groups of 10, 13, 12 and 10 pregnant 

female ITRC-bred albino mice were administered daily 0, 250, 500 and 1,000 ppm of potassium 

33


dichromate (equivalent to doses of approximately 0, 60, 120 and 230 mg/kg/day (0, 20, 40 and 80 

mg Cr (VI)/kg/day)) in drinking water during gestation from day 0 (vaginal plug identified) to day 

19 when dams were sacrificed. At sacrifice, fetuses were subjected to routine external, visceral and 

skeletal examination, and levels of total chromium in the maternal blood, in the placenta and in the 

fetuses were measured. 

No deaths or clinical signs of toxicity were observed in any of the treated dams. Compared to 

controls, a statistically significant reduction in maternal body weight gain of 21% was seen at 500 

ppm, while at 1,000 ppm, a body weight loss of 4% was recorded. Body weight gain was also 

reduced by 18% at 250 ppm, although it did not attain statistical significance. No litters were 

produced at the top dose. Also, 3 females of the low-dose group and 2 females of the middose group 

did not have any litters. A dose-related (statistically significant in the mid-and highdose groups) 

increase in pre-implantation loss was seen across treated groups. There were no implantations 

(100% pre-implantation loss) in the dams treated with 1,000 ppm. Statistically significantly 

increased incidences of post-implantation losses and resorptions were observed at 250 and 500 ppm. 

There was also a dose-related (statistically significant in the mid-dose group) reduction in litter size 

at 250 and 500 ppm. Fetal weight and crown-rump length were statistically significantly reduced in 

the low- and mid-dose groups. No malformations or major skeletal abnormalities were observed. A 

statistically significant increased incidence of kinky tail and subdermal hemorrhagic patches and/or 

streaks on the snout, limbs, back, neck and tail was seen at 500 ppm. A statistically significantly 

reduced ossification in the phalangeal, sternebral, cranial, thoracic and caudal bones was observed 

in fetuses of dams treated with 500 ppm. Fetal cranial ossification was also significantly reduced at 

250 ppm. No significant abnormalities were seen during soft tissue examinations in any of the 

treated groups. Total chromium levels were significantly increased above levels in the control group 

for the maternal blood at 500 and 1,000 ppm, for the placenta at 250 and 500 ppm and for the fetal 

tissues at 500 ppm. 

The complete absence of implantations seen at 1,000 ppm was associated with marked maternal 

toxicity (body weight loss). A range of adverse effects on development was noted at 500 ppm. 

These effects occurred at a dose level at which there was a maternal body weight gain reduction of 

21%. However, since this reduction in body weight gain can be explained by the reduced litter size 

and the reduced fetal weight reported at this dose level, these findings may represent a direct effect 

of potassium dichromate on development. At 250 ppm, adverse effects on development (increased 

incidence of post-implantation losses and resorptions, reduced fetal weight, decreased crown-rump 

length and delayed cranial ossification) were observed in the absence of significant maternal 

toxicity and in association with significant placental levels of total chromium. It can be concluded 

from the results of this study that oral administration of potassium dichromate through drinking 

water to pregnant mice caused fetotoxic effects even at dose levels (250 and possibly 500 ppm) at 

which no maternal toxicity was observed. Thus, a NOAEL value of 120 mg/kg/day (40 mg Cr 

(VI)/kg/day) for maternal toxicity can be identified from this study, but no NOAEL can be 

identified for developmental effects as adverse effects were reported even at the lowest dose tested 

of 60 mg/kg/day (20 mg Cr (VI)/kg/day). 

Junaid et al. (Junaid M. et al., 1996a) exposed pregnant Swiss albino mice (10 per group) to 0, 250, 

500 or 750 ppm potassium dichromate in drinking water during days 6-14 of gestation. Dams were 

subject to caesarean section on day 19 and fetuses examined. Based on average daily water intakes, 

chromium levels received were and 2.00, 3.75 and 5.47 mg/mouse/day. Based on a bodyweight of 

30 g, the estimated intake of potassium dichromate was 190, 350 and 520 mg/kg/day (70, 125 and 

180 mg Cr (VI)/kg/day). There were no maternal deaths or clinical signs of toxicity but weight gain 

was decreased at 350 and 520 mg/kg/day (125 and 180 mg Cr (VI)/kg/day) (reductions of 8.2 and 

34


24% respectively). The number of fetuses per litter was statistically significantly decreased by 20 

and 18%, fetal weight was decreased (by 13 and 20% respectively compared to controls) and the 

number of dead fetuses increased (3 in 2 litters, 12 in 7 litters respectively) at 350 and 520 

mg/kg/day (125 and 180 mg Cr (VI)/kg/day). Post implantation loss increased to statistically 

significant levels of 22 and 34% at 350 and 520 mg/kg/day (125 and 180 mg Cr (VI)/kg/day). 

Reduced ossification, incidence of dropped wrist and subdermal haemorrhagic patches were 

increased at these dose levels. Overall, chromium (VI) caused fetotoxicity but not malformations at 

350 mg/kg/day (125 mg Cr (VI)/kg/day), a dose level which did not produce overt signs of maternal 

toxicity but caused a small decrease in bodyweight gain. The NOAEL for fetal effects was 190 

mg/kg/day (70 mg Cr (VI)/kg/day). 

Other studies 

In a study (Junaid M. et al., 1996b) specifically performed to assess the effect of pregestational 

exposure to chromium on development, groups of 15 female Swiss albino mice of proven fertility 

were administered daily 0, 250, 500 or 750 ppm potassium dichromate (equivalent to doses of 

approximately 0, 63, 119 and 174 mg/kg/day (0, 20, 40 and 60 mg Cr (VI)/kg/day) in drinking 

water for 20 days. The animals were then immediately mated for 24 hours with untreated males, 

and, subsequently, 10 pregnant females were randomly selected from each group and sacrificed on 

day 19 of gestation. Both ovaries were removed from the dams to determine the number of corpora 

lutea. Numbers of implantations and resorptions were recorded and the fetuses were subjected to 

routine external, visceral and skeletal examination. In addition, at sacrifice, levels of total chromium 

in the maternal blood, in the placenta and in the fetal tissues were measured. 

No clinical signs of toxicity were observed in any of the treated females. Mortality (3/15) was noted 

at the top dose. Although autopsy of these animals could not establish the cause of death, given the 

number of deaths and the fact that they occurred at the highest dose, they are likely to be treatmentrelated. 

Body weight gain was unaffected during the treatment. However, during gestation, almost 

no body weight gain was seen in the top-dose dams, and a reduction in body weight gain of 14% 

was observed in the mid-dose dams. Compared to controls, a statistically significant reduction in the 

number of corpora lutea of 44% was noted at 750 ppm. Also, no implantations were seen in this 

group. The number of implantations was also statistically significantly reduced (by 29% of the 

control value) in the dams pregestationally treated with 500 ppm potassium dichromate. A doserelated 

(statistically significant in the mid-dose group) increase in pre-implantation loss was seen at 

250 and 500 ppm. Statistically significantly increased incidences of post-implantation losses were 

observed at 250 and 500 ppm, and of resorptions at 500 ppm. Fetal weight and crown-rump length 

were statistically significantly reduced in the low- and mid-dose groups. There was also a doserelated 

(statistically significantin the mid-dose group) reduction in litter size at 250 and 500 ppm. 

No malformations or major skeletal abnormalities were observed. A statistically significant 

increased incidence of kinky tail, short tail and subdermal hemorrhagic patches was seen at 500 

ppm. A statistically significant reduced ossification in the parietal, interparietal and caudal bones 

was observed in fetuses of dams pregestationally treated with 500 ppm. Fetal caudal ossification 

was also significantly reduced at 250 ppm. No significant abnormalities were seen during soft tissue 

examinations in any of the treated groups. Total chromium levels were significantly increased 

above levels in the control group for the maternal blood in all the treated groups, for the placenta at 

250 and 500 ppm and for the fetal tissues at 500 ppm. 

Overall, the results of this study indicate that pregestational oral administration through drinking 

water of potassium dichromate for 20 days to female mice produced adverse effects on female 

fertility (reduced number of corpora lutea and/or increased pre-implantation loss) at 500 ppm (119 

mg/kg/day (40 mg Cr (VI)/kg/day)) and above. Fetotoxic effects were also seen starting from the 

lowest dose level tested, 250 ppm (63 mg/kg/day (20 mg Cr(VI)/kg/day)). Significant maternal 

35


toxicity (mortality) was observed at 750 ppm. Body weight gain was also dramatically reduced at 

this dose level. However, it is noted that this reduction was mainly due to the complete absence of 

implantations. No significant maternal toxicity was seen at the low and middose levels. Although 

there was a reduction in body weight gain of 14% at 500 ppm, this was accounted for by the 

reduced litter size and the reduced fetal weight. It is finally noted that significant levels of total 

chromium were found in all treated animals at sacrifice, i.e. at around 21 days after the end of the 

treatment. NOAEL values of 119 mg/kg/day (40 mg Cr (VI)/kg/day) and 63 mg/kg/day (20 mg Cr 

(VI)/kg/day) can be identified from this study for maternal toxicity and fertility effects respectively. 

No NOAEL can be identified for developmental effects. Developmental toxicity including 

increased post-implantation losses and resorptions, reduced litter size, fetal weight and crown-rump 

length, increased incidence of kinky tail, short tail and subdermal hemorrhagic patches, and delayed 

ossification of the parietal, interparietal and caudal bones, occurred even in the absence of maternal 

toxicity. 

1.9.3 Human data 

A poorly reported study of the course of pregnancy and childbirth in a group of women employed in 

a chromate production plant produced inconclusive results. Another study claimed that a group of 

women engaged in the production of “chromium compounds” showed a much greater incidence of 

pregnancy complications in comparison with a control group without occupational exposure to 

chromium. The type of exposure to chromium was not specified and the study is of poor quality. No 

conclusions can be drawn regarding any potential effects of chromium on reproduction in humans 

due to the poor quality of the investigations conducted. 

1.9.4 Summary and discussion of reproductive toxicity 

Human data relating to effects on reproduction are limited to poorly reported studies of female 

workers from which no conclusions can be drawn. There are three animal studies available which 

focus on fertility and developmental effects. Adverse effects were produced in mice receiving 

potassium dichromate for 12 weeks in drinking water at 333 mg/kg/day (120 mg Cr (VI)/kg/day) 

and 400 mg/kg/day (140 mg Cr (VI)/kg/day) and above in males and females respectively. A 

NOAEL of 166 mg/kg/day (60 mg Cr (VI)/kg/day) was identified in males but no NOAEL was 

found for females as 400 mg/kg/day was the lowest dose level tested. An increase in resorptions 

following treatment of males and a decrease in implantations in treated females were among the 

findings in this study. In another study, pregestational oral administration of potassium dichromate 

in drinking water to female mice produced adverse effects on fertility (reduced number of corpora 

lutea and increased pre-implantation loss) at 500 ppm (119 mg/kg/day (40 mg Cr (VI)/kg/day)) and 

above. NOAEL values of 119 mg/kg/day (40 mg Cr (VI)/kg/day) and 63 mg/kg/day (20 mg Cr 

(VI)/kg/day) can be identified from this study for maternal toxicity and fertility effects respectively. 

In a third study, fetotoxicity, including post-implantation losses, has been observed in the mouse 

following administration of potassium dichromate in drinking water during gestation (days 0-19). 

Significant developmental effects occurred at the lowest dose level tested, 60 mg/kg/day (20 mg Cr 

(VI)/kg/day) in the absence of maternal toxicity. Therefore no developmental NOAEL was 

determined. Qualitatively similar results were obtained in another study in which (350 mg/kg) 

potassium dichromate (125 mg Cr (VI)/kg) was administered for a shorter period, on days 6-14 of 

gestation. 

Overall, highly water-soluble chromium (VI) compounds should be considered to be developmental 

toxicants in the mouse. These findings can be regarded as relevant to humans. 

36


It is noted that some of the adverse effects on reproduction observed in animal studies may be 

related to the germ cell mutagenicity of these chromium (VI) compounds (see Mutagenicity 

section). 

No reproductive toxicity studies are available using the inhalation or dermal routes of exposure. 

1.10 Other effects 


1.11 Derivation of DNEL(s) or other quantitative or qualitative measure for dose response 


37


2 Annex II : Overall description of chromium manufacturing and chromium uses 

Following information has been compiled and summarized from HSDB (HSDB, 2005) (general 

entry for chromium ions and inorganic and organic chromium compounds), the European Risk 

Assessment Report (E.C., 2005) and from the following industrial websites: 

- http://www.elementischromium.com/products/manufacturing.htm 

- http://www.icdachromium.com/home.php# 

2.1 Manufacture 

Chromium is mined outside of the EU as chromite (FeCr2O4) ore which contains trivalent chromic 

oxide and this is oxidised to sodium chromate during kiln roasting in the chromate-producing 

industry (SCOEL, 2004). Chromite ore and soda ash (sodium carbonate) and sometimes ground 

lime, limestone or dolomite are the principal raw materials in the manufacture of chromium 

chemicals. These compounds are subjected to a high temperature calcination process to produce 

sodium chromate. The vast majority of sodium chromate produced is then reacted with sulphuric 

acid to produce sodium dichromate liquor with sodium sulphate as a co-product. The sodium 

dichromate is used as the derivative to manufacture the whole range of chromium based chemicals. 

Process of manufacturing is illustrated in Figure A1. Hexavalent compounds, with the exception of 

some small amounts in minerals, do not occur naturally in the environment but are formed from 

trivalent chromium during chromate-production processes. 

Only one EU producer has been listed since 2004 in UK and only manufactured sodium dichromate. 

This plant has closed down in 2009. Main manufacturers are now located in South Africa and main 

EU importers are located in UK. Companies wishing to use chromate compounds must use 

imported sources. 

2.2 Main applications and uses of chromium and chromium compounds referenced in 

literature 

Three main sectors of activity using chromium compounds can be distinguished. 

2.2.1 Alloy and chromium metal production 

Of the world's total production of chromite, approximately 95% is smelted into ferrochromium 

alloys. These are for subsequent use in the stainless steel, steel and other alloy industries. 

Chromium metal, composed of nearly 100% chromium, is produced by the aluminothermic or 

electrolytic process. It is mainly used for specialty alloys. 

Main uses referenced by HSDB (HSDB, 2005) are fabrication of alloys, preparation of alloy steels 

to enhance corrosion and heat resistance and production of non-ferrous alloys to impart special 

qualities to the alloys. 

2.2.2 Refractory applications 

Production of chromite for refractory use and foundry sands is about 3% of world production of 

chromite. Refractory chromite is used in sectors of ferrous and non-ferrous metallurgy, in cement 

38


kilns and in the glass industry. Pure chromium oxide is used alone or together with alumina, 

zirconia and silica for high temperature and attack resistant refractories. 

2.2.3 Chromium chemicals manufacturing and related uses 

2% of the world's production of chromite was used in 2008 for manufacturing a variety of 

chromium chemicals (including chromium (VI) compounds) from conversion of sodium chromate 

(sodium dichromate, ammonium and potassium dichromate, chromic acid, chromic oxide and basic 

chromium sulphate, etc.). 

The earliest use of chromium chemicals was during or before the 19 th century for colour and 

pigment applications, due to their very bright colours in clear yellow, orange, green, turquoise and 

blue. Main uses referenced by HSDB are manufacturing of coloured pigments used in dyes, paints 

and plastics, ceramics, cements, papers, rubbers, composition floor covering, surface finishes and 

other materials. 

The second largest use of chromium chemicals is in the metal finishing industry. Chromium is 

actually known for its luster when polished and its protection when coated on metal surfaces. It is 

used as a protective, decorative and increased wear resistance by coating in the sector of metal 

finishing on vehicles parts, plumbing fixtures, furniture parts and many other items, usually applied 

by electroplating. 

Chromium is also regarded with great interest because of its high corrosion resistance and hardness. 

A major development was actually the discovery that steel could be made highly resistant to 

corrosion and discoloration by adding chromium and nickel to form stainless steel and special high 

chromium content super-alloys used in gas turbine engines. Besides decorative plating, hard 

chromium plating is applied extensively to corrosion and wear resistant engineering surfaces and to 

pickling of plastics. Chromium plating is usually made from chromic acid. Stainless steel 

manufacturing and chrome (electro)plating are currently the highest-volume uses of chromium. 

Primer paints containing hexavalent chromium is still widely used for aerospace and automobile 

fishing applications regarding the resistance to corrosion. 

Other smaller uses are the following: 

- mordant in textile industry in dyeing silk treating, printing, and moth proofing wool, 

- tanning in leather industry, 

- fixing baths in photographic, 

- catalytic manufacture (catalysts for halogenation, alkylation, and catalytic cracking of 

hydrocarbons, etc.) 

- fuel additives and propellant additives in ceramics, 

- fabrication of magnetic tapes, 

- use in cooling “fluids”, 

- use in wood preservatives, 

- use in medicine as astringents and antiseptics, 

- etc. 

This multiplicity of uses explains that chromium is commonly found in a wide range of articles such 

as aircrafts, motorcars, barrels, buses, cans, electrical appliances, flatware, hardware, lumber, 

pharmaceuticals, pigments and dyes, railroad equipment, ships, etc. 

39


Specific application in wood preservation: 

Potassium dichromate, sodium dichromate and chromium trioxide have been used in the 

formulation of water-borne wood preservatives for about a century (ICDA, 1998). They function as 

essential chemical fixatives for the copper and other fungicidal and insecticidal components in the 

widely used chromated-copper preservatives, of which the best known example is CCA (copperchrome-arsenic 

mixture). Studies have shown that chromium in these preservatives has little or no 

direct action against decay fungi. However, stabilisation of the other preservative components 

achieved through valency state reduction of chromium makes them resistant to leaching and 

provides the treated wood with long-term durability against fungal and insect attack, even in high 

risk environments. It should be noted that chromium compounds have virtually no fungicidal (or 

insecticidal) activity in wood. Despite the long and successful history of use of chromate containing 

wood preservatives, a number of regulatory authorities have and are considering restrictions or bans 

on their use for certain products; interestingly, CCA preservatives are still permitted for timber for 

export and for local heavy duty applications. 

Now, the use of potassium dichromate and sodium dichromate in the formulation of wood 

preservatives is not allowed in Europe following European Commission decision of the 5 th of 

December 2007 on the basis of the 27 th meeting of representatives of Member States Competent 

Authorities for the implementation of Directive 98/8/EC concerning the placing of biocidal products 

on the market (“Way forward on chromium”). The harmonized approach taken is the following: in 

order to ensure that chromic acid in wood preservatives has none or a negligible biocidal activity, 

chromium-containing wood preservatives meeting the following requirements on their composition 

and use shall be allowed to remain on the market. No other form than chromic acid (chromium 

trioxide) should be allowed in the product. Other chromium compounds, such as potassium 

dichromate or sodium dichromate should not be allowed, as no data have been provided to 

demonstrate that these compounds have no, or only a negligible, biocidal activity. This approach 

has however not been endorsed by several countries (UK, IE, LT and HU). 

40


Chromite 

Figure A1: Example of chromium compounds manufacturing process (from ICDA website) 

41


3 Annex III: Treatment and coating of metals, metal finishing processes using 

chromium (VI) compounds 

The main process which involves chromium is electroplating (chrome plating), but other uses are in 

conversion coatings (passivating and anodising) and in brightening (E.C., 2005). The electroplating 

sector constitutes approximately 43% of the total number of companies with metal finishing 

activities. 

According to the industry (French consultation, 2010), main activities of the metal finishing sector 

using chromate compounds are anodising application, chemical and electrolytic coatings and paints, 

which represent respectively 5%, 24% and 32% of the total metal finishing activity. Main purposes 

of metal treatments are appearance improving (12%), resistance to corrosion (46%), wear resistance 

(24%) and others (electrical conductivity, etc.). 

The distribution of chromium (VI) compounds used by metal finishing workshops to prepare 

treatment baths (all merged processes) was in 2004 according to the French Metal Finishing Trade 

Union: 

• chromium trioxide 64% (meaning that 64% of all metal treatment baths are prepared from 

chromium trioxide), 

• potassium dichromate 17%, 

• sodium dichromate 17%, 

• ammonium dichromate 2%, 

• potassium chromate 2%. 

3.1 Formulation of metal treatment products 

There are many different companies throughout the EU who make formulations for use in metal 

treatment (E.C., 2005). The formulations are usually confidential. However, the same two basic 

mixing processes are used to manufacture them: dry mixes or liquid mixes. The process is 

essentially one of mixing components together into a product and then packaging. Chromium 

trioxide is the most common chromium (VI) compound used. 

3.2 Conversion coating (usually called chromate conversion coating – CCC) or 

chromating 

Conversion coatings are produced by the chemical treatment of metallic surfaces to give a barrier 

layer of complex chromium compounds on the metal surface, to protect the base metal from 

corrosion (E.C., 2005). It can also provide a good base for subsequent painting, give a chemical 

polish and/or colour the metal. 

There is a range of processes which fit under this heading; the two involving chromium compounds 

are passivating and anodising. Passivating is a chemical treatment applied to a metal product to 

enhance corrosion resistance whereas anodising is an electrolytic process designed to produce an 

oxide film integral with the surface of the metal. The compositions of the treatment baths are 

proprietary and can vary greatly and may contain either chrome (VI) or chrome (III). The coatings 

can be applied either by immersion or electrolytically (E.C., 2005). 

Chromate conversion coating is a type of conversion coating applied to passivate aluminium, zinc, 

cadmium, copper, silver, magnesium, tin and their alloys to slow corrosion and to make metalplated 

parts more durable. The strong oxidative properties of chromates are used to deposit a 

protective oxide layer of complex chromium compounds on metallic surfaces to protect the base 

42


metal from corrosion. This passivation and the self healing properties by the chromate stored in the 

chromate conversion coating, which is capable to migrate to local defects, are the benefits of this 

coating method. It can also provide a good base for subsequent painting, give a chemical polish 

and/or colour the metal. 

The chromate coating acts like a paint, protecting the zinc from white corrosion, this can make the 

part several times more durable depending on chromate layer thickness. It cannot be applied 

directly to steel or iron, and does not enhance zinc's cathodic protection of the underlying steel from 

brown corrosion. It is also commonly used on aluminium alloy parts in the aircraft industry where it 

is often called chemical film, or the well known brand name Alodine. It has additional value as a 

primer for subsequent organic coatings, as untreated metal, especially aluminium, is difficult to 

paint or glue. Chromated parts retain their electrical conductivity to varying degrees, depending on 

coating thickness. The process may be used to add color for decorative or identification purposes. 

Coating thickness vary from a few nanometers to a few micrometers thick. 

The protective effect of chromate coatings on zinc is indicated by color, progressing from clear/blue 

to yellow, gold, olive drab and black. Darker coatings generally provide more corrosion resistance. 

Chromate conversion coatings are common on everyday items such as hardware and tools and 

usually have a distinctive yellow color. 

The composition of chromate conversion solutions varies widely depending on the material to be 

coated and the desired effect. Most solution compositions are proprietary. The widely used Cronak 

process for zinc and cadmium consists of 5–10 seconds of immersion at room temperature in a 

solution of 182 g/L sodium dichromate crystals (Na2Cr2O72H2O) and 6 mL/L concentrated sulfuric 

acid. 

Anodising of aluminium is an electrolytic passivation process used to increase the thickness of the 

natural oxide layer on the surface of metal parts. Anodising increases corrosion resistance and wear 

resistance, and provides better adhesion for paint primers and glues than bare metal. The most 

widely used anodising specification, MIL-A-8625, defines three types of aluminium anodisation: 

Type I is chromic acid anodisation, Type II is sulfuric acid anodisation and Type III is sulfuric 

acid hardcoat anodisation. The oldest anodising process uses chromic acid which does not lead to 

the deposition of chromium but uses chromic acid as electrolyte in the solution. It is widely known 

as the Bengough-Stuart process. In the UK it is normally specified as Def Stan 03/24 and used in 

areas that are prone to come into contact with propellants etc. There are also Boeing and Airbus 

standards. Chromic acid produces thinner, 0.5 µm to 18 µm more opaque films that are softer, 

ductile, and to a degree self-healing. They are harder to dye and may be applied as a pretreatment 

before painting. A sealing is usual needed after anodising and uses different processes, particularly 

potassium dichromate salt (please see infra). 

3.3 Sealing after anodising 

Acidic anodising solutions produce pores in the anodised coating. These pores can absorb dyes and 

retain lubricants, but are also an avenue for corrosion. When lubrication properties are not critical, 

they are usually sealed after dyeing to increase corrosion resistance and dye retention. Different 

types of sealing exist. Teflon, nickel acetate, cobalt acetate, and hot sodium or potassium 

dichromate seals are commonly used. Dichromate compounds are often used for this purpose in the 

aeronautic sectors which use aluminium alloys 2024 and 2019. 

43


3.4 Chrome (electro)plating or chrome dipping or chroming 

Chrome plating, often referred to simply as chrome, is a technique of electroplating a thin layer of 

chromium onto a metal object. Chrome is only applied by electroplating. Chromium plating is 

mainly done either to increase resistance to rust and corrosion, to facilitate cleaning procedures, to 

increase surface hardness and resistance to wear and tear (hard chrome plating) or for decoration 

and aesthetic reasons, in order to achieve a shining surface (decorative chrome plating). The surface 

thickness for the former is typically 10 to 1000 µm, for the latter, between 0.25 and 1.0 µm. 

3.4.1 Chrome plating methods 

There are two types of industrial chrome plating solutions: 

1. Hexavalent chromium baths which main ingredient is chromic anhydre. When mixed with 

acid, chromate ions CrO4 2- , first form dichromate ions Cr2O7 2- , then chromic acid H2CrO4. 

Solutions containing chromic acid are powerfully oxidizing and highly corrosive. 

2. Trivalent chromium baths whose main ingredient is chromium sulfate or chromium chloride 

The component will generally go through these different stages. 

• Degreasing to remove heavy soiling. 

• Manual cleaning to remove all residual traces of dirt and surface impurities. 

• Various pretreatments depending on the substrate. 

• Placed into the chrome plating vat and allowed to warm to solution temperature. 

• Plating current applied and component is left for the required time to attain thickness. 

There are four methods of chromium plating: barrel; manual; semi-automatic and automatic (E.C., 

2005). 

Barrel plating is used for plating small parts at low cost. Either the parts and solution are rotated 

together in an open-ended barrel or parts are enclosed in a cage and transferred manually or 

automatically from one plating solution to another. The advantages of using barrel plating are low 

cost and a more enclosed process, so reducing exposure to the plating solutions. 

Manual plating is a series of tanks that contain the appropriate plating and cleaning solutions. Parts 

are placed on racks or hangers and manually transferred from tank to tank. This type of plating 

process is labour intensive and, as platers spend a larger proportion of their working time at the 

tanks, there is a relatively higher risk of exposure. However, the use of this method is declining 

because of the high costs associated with labour intensive processes. 

In semi-automatic plating, parts are manually loaded on to jigs and then the operator moves the jigs 

between the baths using an overhead hoist in a predetermined sequence. The operator usually stands 

on a platform by the side of the plating line. This method usually results in lower exposure than 

manual plating as the operators can distance themselves from the plating solutions for large 

amounts of time. 

The main difference between automatic and semi-automatic plating is that the movement of the jigs 

is controlled electronically in automatic plating and therefore the operator spends very little time 

near the plating solutions, except when there is a problem with the process. 

44


3.4.2 Chrome plating processes 

There are two main distinct types of chromium plating processes; decorative and hard chrome 

plating. It is possible to use chromium (III) salts for decorative chrome plating and there has been 

an increase in chromium (III) decorative plating in recent years at the expense of chromium (VI) 

decorative plating (E.C., 2005). 

Hard chrome plating is chrome plating that has been applied as a fairly heavy coating (usually 

measured in thousandths of an inch) for wear resistance, lubricity, oil retention, and other 'wear' 

purposes. Some examples would be hydraulic cylinder rods, rollers, piston rings, mold surfaces, 

thread guides, gun bores, etc. 'Hard chrome' is not really harder than other chrome plating, it is 

called hard chromium because it is thick enough that a hardness measurement can be performed on 

it, whereas decorative chrome plating is only millionths of an inch thick and will break if a hardness 

test is conducted, so its hardness cannot really be measured directly. 

Decorative chrome plating is sometimes called nickel-chrome plating because it always involves 

electroplating nickel onto the object before plating the chrome (it sometimes also involves 

electroplating copper onto the object before the nickel, too). The nickel plating provides the 

smoothness, much of the corrosion resistance, and most of the reflectivity. The chrome plating is 

exceptionally thin, measured in millionths of an inch rather than in thousandths. Nickel plating is 

the main touch of a decorative chrome plated surface (such as a chrome plated wheel or truck 

bumper). The chrome adds a bluish cast (compared to the somewhat yellowish cast of nickel), 

protects the nickel against tarnish, minimizes scratching, and symbiotically contributes to corrosion 

resistance. Without such nickel undercoating no reflective and decorative surface is possible. 

The most important issue for durable chrome plating for outdoor exposure such as on a vehicle is 

that at least two layers of nickel plating are needed before the chrome layer called "duplex nickel 

plating": semi-bright nickel followed by bright nickel. The reason for this involves galvanic 

corrosion issues. The bright nickel is anodic to the semi-bright nickel, and sacrificially protects it, 

spreading the corrosion forces laterally instead of allowing them to penetrate through to the steel. 

Electrolytic chromium/chromium oxide coated steel (E.C., 2005) 

Steels used in packaging, e.g. cans, are non-alloyed steel flat products and are used for drinks or 

food products. Depending on the application, the steel can be covered with a metal coating (tin or 

chromium) or with an additional organic coating. The two main steels used for packaging products 

are tinplate and electrolytic chromium coated steel (ECCS). Their technical specifications are 

described in EN10202. They are both certified for food contact materials. After tinning, tinplate is 

subject to a passivation treatment in which chromium and chromium oxides are deposited on to the 

surface, to improve resistance to oxidation and improve suitability for lacquering and printing. The 

most widely used passivation process for tinplate is a cathodic treatment in a solution of sodium 

dichromate (3.5 to 9 mg/m 2 ). ECCS is always used lacquered. On the surface of the strip a coating 

mass between 50 and 140 mg/m 2 (total chromium) is applied. Chromium (VI) is used in both 

processes, but is reduced to chromium metal and chromium (III) on the final product. Consumer 

exposure to chromium (VI) is therefore likely to be negligible from this source. 

45


3.4.3 Brightening 

This process may be part of the surface preparation before a major process such as electroplating. 

Chromates are used only for copper, zinc and their alloys. Brightening basically involves dipping 

the substrate into a solution of chromium salts to remove scale, oxide films and tarnish. Chromate 

baths are not normally made up specifically for this purpose, but where a bath is already made up 

for plating or other use it may also be used for this purpose (E.C., 2005). 

46


4 Annex IV: Uses of chromium (VI) salts in the textile sector (process) 

This information is drawn from the Italian Textile and Health Association (Associazione Tessile e 

Salute, 2009). The entire document focuses on the use of sodium dichromate in dyeing of textile 

fibres (processes, control of human exposure - workers during the process and consumer through 

the articles-, control of environment exposure, waste management, etc.). This information is 

expected to be also valid for other Cr (VI) compounds used for the same purpose and process. 

4.1 Dyeing of protein fibres 

The use of sodium dichromate is based on a oxidation-reduction reaction which transforms the 

hexavalent chromium chemical into the corresponding trivalent chromium, with following creation 

of a stable complex between this and the dyeing molecule uniformly diffused and chemically bound 

inside the fibres. 

Furthermore, hexavalent chromium added in the dyeing bath totally binds to the fibre as it does not 

exceed the material thanks to the stoichiometric dyeing method adopted. 

The percentages to use according to the material weight vary between 0.1 and 3% of solution 

dichromate. The process is divided into three phases: 

- First phase: ordinary dyeing with acid dyes 

- Second phase: the called “chromating” process, which uses sodium dichromate, working at a 

temperature of 94-96°C for a variable time between 30 and 40 minutes 

- Third phase: reduction (with thiosulphate and/or washing). 

The dyeing and chromating processes are carried out in closed containers whereas the exhausted 

dyeing baths are drained through pipes which ensure their transport to the company’s and /or 

cooperative depuration system. 

When applied to tops, the dyed material often undergoes further washing with ammonia and soap at 

a temperature between 30 and 40°C in continuous machines, called “backwashing machines”, 

which guarantee the fibre sliver to be deeper cleaned during the transport to the company’s or 

cooperative depuration plant. 

The chemical agent is used as a solution and this strongly limits the risks for the operators; in fact 

the main risk is represented by inhalation and being the agent vapour tension in the form of metal 

ion practically void, its presence as aerosol in the working place is quite improbable. 

Moreover, a deliberate exposure by skin contact or ingestion is absolutely to exclude because eating 

and/or drinking is strictly forbidden in the working place, also with regard to how the chemical 

agent is used in a closed system. 

The closed circuit dosing system is equipped with a storage tank, into which the external supplier 

let the liquid chemical agent flow; this tank must be positioned in such a way so as to ensure 

conveyance of any accidental release to the depuration plant and to prevent its drying. The dosing 

system must also be equipped with highly precise volumetric weighing system and automatic 

distribution to the dying devices by means of a piping network. 

In the rare event that the quantity of sodium dichromate to be used is so small that the automatic 

dosing system cannot be employed (dyeing of minimum quantities or lab tests), all the operations 

shall be carried out with the aid of personal protection devices like nitril gloves, glasses, mask. 

47


Furthermore, it can be affirmed that at the end of the dyeing cycle, when the textile is still inside the 

dyeing apparatus and prior to sampling (when the colour compliance is checked), the whole 

quantity of hexavalent chromium has been already reduced to trivalent chromium as a security for 

the operators. 

4.2 Chemical reaction with fibre and dyestuff 

Cr (III) salt is not used as mordant since the treatment should take place in acid environment and at 

such conditions that wool with protonatized sites would not only bind with Cr³ + ions but on the 

contrary would tendentially repel them. This is the reason why Cr 6+ as Cr2O7 — . anion is used. 

Reacting with dichromate in acid environment, Cr2O7 — anion is first fixed by ionic bond to the 

protonatized amino groups of the wool and then reduced by reaction with wool reducing groups, 

among which the -S-S- cystine group: 

Cr2O7 -- + 6 and - + 14 H + ↔ 2 Cr 3+ + 7 H2O 

Now Cr 3+ ion is already distributed inside the fibre and can bind with - COOH groups of the wool 

and form complexes with the dye, furthermore with a less acid pH it can also bind with the amino 

compounds of the fibre by means of coordinative linking. 

In practice, there take place the simultaneous Cr 6+ reduction and Cr 3+ combination with the dye in 

the fibre. 

In this way the Cr (III) ion works as linking species between fibre and dye, and this explains the 

high colour fastness levels obtained with these dyes. 

4.3 Subsequent processes 

The need to assess also the processes downstream the dyeing cycle is due to the assumption that 

should a residual part of hexavalent chromium be present inside the dyed material, this could cause 

exposure to inhalation by the operators in the downstream production areas because of the 

formation of fibrous particulate caused by mechanical operations, like for example the blending of 

top slivers. 

Actually, the stoichiometric use of the chemical agent according to the type and quantity of the 

material to be processed and to the dye intensity implies the almost total absence of residual 

hexavalent chromium inside the dyed textile. 

48

Annex XV dossier PROPOSAL FOR IDENTIFICATION OF A ... - ECHA

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